Frequency Range Of Sleep Spindles Research Articles

Nocturnal Brain Activity Differs with Age and Sex: Comparisons of Sleep EEG Power Spectra Between Young and Elderly Men, and Between 60-80-Year-Old Men and Women.

PurposeQuantification of nocturnal EEG activity has emerged as a promising extension to the conventional sleep evaluation approach. To date, studies focusing on quantitative sleep EEG data in relation to age and sex have revealed considerable variation across lifespan and differences between men and women. However, sleep EEG power values from elderly individuals are still rare. The present secondary analysis aimed to fill this gap.Participants and MethodsSleep EEG data of 30 healthy elderly males (mean age ± SD: 69.1 ± 5.5 years), 30 healthy elderly females (67.8 ± 5.7 years), and of 30 healthy young males (25.6 ± 2.4 years) have been collected in three different studies with the same experimental design. Each individual contributed three polysomnographic recordings without any intervention to the analysis. Sleep recordings were performed and evaluated according to the standard of the American Academy of Sleep Medicine. Sleep EEG signals were derived from 19 electrode sites. Sleep-stage specific global and regional EEG power were compared between samples using a permutation-based statistic in combination with the threshold-free cluster enhancement method.ResultsThe present results showed pronounced differences in sleep EEG power between older men and women. The nocturnal EEG activity of older women was generally larger than that of older men, confirming previously reported variations with sex in younger individuals. Aging was reflected by differences in EEG power between young and elderly men for lower frequencies and for the sleep spindle frequency range, again consistent with prior studies.ConclusionThe findings of this investigation complement those of earlier studies. They add to the understanding of nocturnal brain activity manifestation in senior adulthood and show how it differs with age in males. Unfortunately, the lack of information on young women prevents a similar insight for females.

Different maturational changes of fast and slow sleep spindles in the first four years of life

Objective/BackgroundMassive changes in brain morphology and function in the first years of life reveal a postero-anterior trajectory of cortical maturation accompanied by regional modifications of NREM sleep. One of the most sensible marker of this maturation process is represented by electroencephalographic (EEG) activity within the frequency range of sleep spindles. However, direct evidence that these changes actually reflect maturational modifications of fast and slow spindles still lacks.Our study aimed at answering the following questions:1. Do cortical changes at 11.50 Hz frequency correspond to slow spindles?2. Do fast and slow spindles show different age trajectories and different topographical distributions?3. Do changes in peak frequency explain age changes of slow and fast spindles? Patients/MethodsWe measured the antero-posterior changes of slow and fast spindles in the first 60 min of nightly sleep of 39 infants and children (0–48 mo.). ResultsWe found that (A) changes of slow spindles from birth to childhood mostly affect frontal areas (B) variations of fast and slow spindles across age groups go in opposite direction, the latter progressively increasing across ages; (C) this process is not merely reducible to changes of spindle frequency. ConclusionsAs a main finding, our cross-sectional study shows that the first form of mature spindle (i.e., corresponding to the adult phasic event of NREM sleep) is marked by the emergence of slow spindles on anterior regions around the age of 12 months.

Slow oscillations during sleep coordinate interregional communication in cortical networks.

Large-amplitude sleep slow oscillations group faster neuronal oscillations and are of functional relevance for memory performance. However, relatively little is known about the impact of slow oscillations on functionally coupled networks. Here, we provide a comprehensive view on how human slow oscillatory dynamics influence various measures of brain processing. We demonstrate that slow oscillations coordinate interregional cortical communication, as assessed by phase synchrony in the sleep spindle frequency range and cross-frequency coupling between spindle and beta activity. Furthermore, we show that the organizing role of slow oscillations is restricted to circumscribed topographical areas. These findings add importantly to our basic understanding of the orchestrating role of slow oscillations. In addition, they are of considerable relevance for accounts of sleep-dependent memory reprocessing and consolidation.

Slow sleep spindle activity, declarative memory, and general cognitive abilities in children.

Functional interactions between sleep spindle activity, declarative memory consolidation, and general cognitive abilities in school-aged children. Healthy, prepubertal children (n = 63; mean age 9.56 ± 0.76 y); ambulatory all-night polysomnography (2 nights); investigating the effect of prior learning (word pair association task; experimental night) versus nonlearning (baseline night) on sleep spindle activity; general cognitive abilities assessed using the Wechsler Intelligence Scale for Children-IV (WISC-IV). Analysis of spindle activity during nonrapid eye movement sleep (N2 and N3) evidenced predominant peaks in the slow (11-13 Hz) but not in the fast (13-15 Hz) sleep spindle frequency range (baseline and experimental night). Analyses were restricted to slow sleep spindles. Changes in spindle activity from the baseline to the experimental night were not associated with the overnight change in the number of recalled words reflecting declarative memory consolidation. Children with higher sleep spindle activity as measured at frontal, central, parietal, and occipital sites during both baseline and experimental nights exhibited higher general cognitive abilities (WISC-IV) and declarative learning efficiency (i.e., number of recalled words before and after sleep). Slow sleep spindles (11-13 Hz) in children age 8-11 y are associated with inter-individual differences in general cognitive abilities and learning efficiency.

Individual differences in the effects of mobile phone exposure on human sleep: Rethinking the problem

Mobile phone exposure-related effects on the human electroencephalogram (EEG) have been shown during both waking and sleep states, albeit with slight differences in the frequency affected. This discrepancy, combined with studies that failed to find effects, has led many to conclude that no consistent effects exist. We hypothesised that these differences might partly be due to individual variability in response, and that mobile phone emissions may in fact have large but differential effects on human brain activity. Twenty volunteers from our previous study underwent an adaptation night followed by two experimental nights in which they were randomly exposed to two conditions (Active and Sham), followed by a full-night sleep episode. The EEG spectral power was increased in the sleep spindle frequency range in the first 30 min of non-rapid eye movement (non-REM) sleep following Active exposure. This increase was more prominent in the participants that showed an increase in the original study. These results confirm previous findings of mobile phone-like emissions affecting the EEG during non-REM sleep. Importantly, this low-level effect was also shown to be sensitive to individual variability. Furthermore, this indicates that previous negative results are not strong evidence for a lack of an effect and, given the far-reaching implications of mobile phone research, we may need to rethink the interpretation of results and the manner in which research is conducted in this field.

Mobile phones and sleep - A review

Mobile phones and sleep - A review The increasing use of mobile phones has raised concerns regarding the potential health effects of exposure to the radiofrequency electromagnetic fields. An increasing amount research related to mobile phone use has focussed on the possible effects of mobile phone exposure on human brain activity and function. In particular, the use of sleep research has become a more widely used technique for assessing the possible effects of mobile phones on human health and wellbeing especially in the investigation of potential changes in sleep architecture resulting from mobile phone use. Acute exposure to a mobile phone prior to sleep significantly enhances electroencephalogram spectral power in the sleep spindle frequency range. This mobile phone-induced enhancement in spectral power is largely transitory and does not linger throughout the night. Furthermore, a reduction in rapid eye movement sleep latency following mobile phone exposure was also found, although interestingly, neither this change in rapid eye movement sleep latency or the enhancement in spectral power following mobile phone exposure, led to changes in the overall quality of sleep. In conclusion, a short exposure to the radiofrequency electromagnetic fields emitted by a mobile phone handset immediately prior to sleep is sufficient to induce changes in brain activity in the initial part of sleep. The consequences or functional significance of this effect are currently unknown and it would be premature to draw conclusions about possible health consequences.

Functional Connectivity between Cortex and Motor Nuclei of the Basal Ganglia across the Human Sleep-Wake Cycle

Functional imaging has shown a basal ganglia involvement in the activity changes across the human sleep-wake cycle. Here we used frequency analysis to explore whether motor nuclei of the basal ganglia (Globus pallidus internus [GPi], subthalamic nucleus [STN]) are functionally connected to the motor or the visual cortex in wakefulness, NREM2, NREM3/4 and REM sleep. To this end, we examined patients undergoing deep-brain stimulation for Parkinson's disease (PD; n=5) or dystonia (n=5). We simultaneously recorded local field potentials either from GPi or STN using a bipolar montage as well as scalp EEG (F3/4-C3/4, Pz-O1/2). Frequency analysis of scalp EEG between motor and visual cortex in GPi patients confirmed previous studies in healthy subjects during sleep (Achermann & Borbély, 1998), whereas in STN patients additional peaks were present in the delta-/theta-frequency range. In the coherence spectra strong peaks can be shown at 12–16Hz between GPI and both motor and visual cortex in NREM2, corresponding to the sleep spindle frequency range. Further, a distinct peak could be identified in the higher alpha-range (10–12Hz). In contrast, in NREM3/4 the 12–16Hz-coherence peak was not present while the 10–12Hz-peak remained. For NREM2 and NREM3/4 the 10–12Hz peak disappeared after partialization of the surface EEG with GPi as the predictor. The directed transfer function (dtf) revealed that the peak at 12–16Hz is predominantly propagated from the visual cortex to GPi and motor cortex in NREM2 and NREM3/4. The dtf for GPi to motor and visual cortex showed a distinct peak in the higher alpha-range (10–12Hz) in NREM2, while in NREM3/4 distinct peaks at 10–12Hz were present between GPi and motor cortex as well as from motor to visual cortex. Principally, the same coherence patterns were also present in STN patients, however at a much lower level and less homogeneously than in GPi patients. There was no significant coherence in REM between STN or GPi and cortex. We can show functional connectivity between motor nuclei of the basal ganglia and both the motor and the visual cortex in NREM sleep in the frequency range of sleep spindles. The motor system seems to be additionally synchronized with a peak in the higher alpha-range (10–12Hz), propagated through the GPi to the cortex. Most likely, the synchronization at 10–12Hz can be regarded as a specific signature of the motor system in NREM sleep, which parallels the overall synchronization at 12–16Hz.

Short- and medium-term plasticity associated with augmenting responses in cortical slabs and spindles in intact cortex of cats in vivo.

Plastic changes in the synaptic responsiveness of neocortical neurones, which occur after rhythmic stimuli within the frequency range of sleep spindles (10 Hz), were investigated in isolated neocortical slabs and intact cortex of anaesthetized cats by means of single, dual and triple simultaneous intracellular recordings in conjunction with recordings of local field potential responses. In isolated cortical slabs (10 mm long, 6 mm wide and 4-5 mm deep), augmenting responses to pulse-trains at 10 Hz (responses with growing amplitudes from the second stimulus in a train) were elicited only by relatively high-intensity stimuli. At low intensities, responses were decremental. The largest augmenting responses were evoked in neurones located close to the stimulation site. Quantitative analyses of the number of action potentials and the amplitude and area of depolarization during augmenting responses in a population of neurones recorded from slabs showed that the most dramatic increases in the number of spikes with successive stimuli, and the greatest increase in depolarization amplitude, were found in conventional fast-spiking (FS) neurones. The largest increase in the area of depolarization was found in regular-spiking (RS) neurones. Dual intracellular recordings from a pair of FS and RS neurones in the slab revealed more action potentials in the FS neurone during augmenting responses and a significant increase in the depolarization area of the RS neurone that was dependent on the firing of the FS neurone. Self-sustained seizures could occur in the slab after rhythmic stimuli at 10 Hz. In the intact cortex, repeated sequences of stimuli generating augmenting responses or spontaneous spindles could induce an increased synaptic responsiveness to single stimuli, which lasted for several minutes. A similar time course of increased responsiveness was obtained with induction of cellular plasticity. These data suggest that augmenting responses elicited by stimulation, as well as spontaneously occurring spindles, may induce short- and medium-term plasticity of neuronal responses.

High doses of systemic DHEA-sulfate do not affect sleep structure and elicit moderate changes in non-REM sleep EEG in rats

The hormone dehydroepiandrosterone (DHEA) and its metabolite DHEA-sulfate (DHEAS) occur in huge quantities in the plasma as well as in the brain of vertebrates. To investigate whether DHEAS modulates sleep-wake behavior, we assessed the sleep response to three doses (25, 50, and 100 mg/kg) of intraperitoneally administered DHEAS, mixed with oil, in 8 rats. DHEAS injections produced dose-dependent and long-lasting elevations in the plasma levels of both DHEAS and DHEA. DHEAS administration did not affect sleep time and architecture but exerted persistent effects on the electroencephalogram (EEG) within non–rapid eye movement sleep: 50 mg/kg DHEAS significantly augmented EEG power in the frequency range of sleep spindles, and 100 mg/kg DHEAS depressed EEG power in the slow-wave frequency bands. The findings indicate that DHEAS changes the sleep EEG in a dose-dependent way, possibly through a modulation of GABA- and glutamate-induced currents.

Frequency and state specific hemispheric asymmetries in the human sleep EEG

Regional differences in the sleep EEG along the antero-posterior axis have been recently described. To test for state related, hemispheric differences, sleep records from homologous fronto-central, centro-parietal and parieto-occipital derivations were obtained from 14 young right-handed males. Within the frequency range of sleep spindles (11–15 Hz) power in non-REM sleep dominated in the left hemisphere in all derivations. In the centro-parietal 4–8 Hz band a right-hemispheric predominance prevailed in non-REM sleep and a left-hemispheric predominance in REM sleep. Since the frequency bands exhibiting hemispheric asymmetries are those in which large antero-posterior power gradients had been observed, the left-right differences may arise from structural and functional asymmetries of brain regions involved in the generation of the sleep EEG.

Temporal evolution of coherence and power in the human sleep electroencephalogram.

Coherence analysis of the human sleep electroencephalogram (EEG) was used to investigate relations between brain regions. In all-night EEG recordings from eight young subjects, the temporal evolution of power and coherence spectra within and between cerebral hemispheres was investigated from bipolar derivations along the antero-posterior axis. Distinct peaks in the power and coherence spectra were present in NREM sleep but not in REM sleep. They were situated in the frequency range of sleep spindles (13-14 Hz), alpha band (9-10 Hz) and low delta band (1-2 Hz). Whereas the peaks coincided in the power and coherence spectra, a dissociation of their temporal evolution was observed. In the low delta band, only power but not coherence showed a decline across successive NREM sleep episodes. Moreover, power increased gradually in the first part of a NREM sleep episode, whereas coherence showed a rapid rise. The results indicate that the intrahemispheric and interhemispheric coherence of EEG activity attains readily a high level in NREM sleep and is largely independent of the signal amplitude.

Variation of electroencephalographic activity during non-rapid eye movement and rapid eye movement sleep with phase of circadian melatonin rhythm in humans.

1. The circadian pacemaker regulates the timing, structure and consolidation of human sleep. The extent to which this pacemaker affects electroencephalographic (EEG) activity during sleep remains unclear. 2. To investigate this, a total of 1.22 million power spectra were computed from EEGs recorded in seven men (total, 146 sleep episodes; 9 h 20 min each) who participated in a one-month-long protocol in which the sleep-wake cycle was desynchronized from the rhythm of plasma melatonin, which is driven by the circadian pacemaker. 3. In rapid eye movement (REM) sleep a small circadian variation in EEG activity was observed. The nadir of the circadian rhythm of alpha activity (8.25-10.5 Hz) coincided with the end of the interval during which plasma melatonin values were high, i.e. close to the crest of the REM sleep rhythm. 4. In non-REM sleep, variation in EEG activity between 0.25 and 11.5 Hz was primarily dependent on prior sleep time and only slightly affected by circadian phase, such that the lowest values coincided with the phase of melatonin secretion. 5. In the frequency range of sleep spindles, high-amplitude circadian rhythms with opposite phase positions relative to the melatonin rhythm were observed. Low-frequency sleep spindle activity (12.25-13.0 Hz) reached its crest and high-frequency sleep spindle activity (14.25-15.5 Hz) reached its nadir when sleep coincided with the phase of melatonin secretion. 6. These data indicate that the circadian pacemaker induces changes in EEG activity during REM and non-REM sleep. The changes in non-REM sleep EEG spectra are dissimilar from the spectral changes induced by sleep deprivation and exhibit a close temporal association with the melatonin rhythm and the endogenous circadian phase of sleep consolidation.

Spindle frequency activity in the sleep EEG: individual differences and topographical distribution

The brain topography of EEG power spectra in the frequency range of sleep spindles was investigated in 34 sleep recordings from 20 healthy young men. Referential (F3-A2, C3-A2, P3-A2 and O1-A2) and bipolar derivations (F3-C3, C3-P3 and P3-O1) along the antero-posterior axis were used. Sleep spindles gave rise to a distinct peak in the EEG power spectrum. The distribution of the peak frequencies pooled over subjects and derivations showed a bimodal pattern with modes at 11.5 and 13.0 Hz, and a trough at 12.25 Hz. The large inter-subject variation in peak frequency (range: 1.25 Hz) contrasted with the small intra-subject variation between derivations, non-REM sleep episodes and different nights. In some individuals and/or some derivations, only a single spindle peak was present. The topographic distributions from referential and bipolar recordings showed differences. The power showed a declining trend over consecutive non-REM sleep episodes in the low range of spindle frequency activity and a rising trend in the high range. The functional and topographic heterogeneity of sleep spindles in conjunction with the intra-subject stability of their frequency are important characteristics for the analysis of sleep regulation on the basis of the EEG.

Effect of age on the sleep EEG: slow-wave activity and spindle frequency activity in young and middle-aged men

The effect of age on sleep and the sleep EEG was investigated in middle-aged men (mean age: 62.0 years) and in young men (mean age: 22.4 years). Even though the older men reported a higher number of nocturnal awakenings, subjective sleep quality did not differ. Total sleep time, sleep efficiency, and slow wave sleep were lower in the middle-aged, while stage 1 and wakefulness after sleep onset were higher. The difference in wakefulness within nonREM-REM sleep cycles was most pronounced in the third and fourth cycle. In the older men, EEG power density in nonREM sleep was reduced in frequencies below 14.0 Hz, whereas in REM sleep age-related reductions were limited to the delta-theta (0.25 – 7.0 Hz) and low alpha (8.25 – 10.0 Hz) band. Slow-wave activity (SWA, power density in the 0.75 – 4.5 Hz range) decreased in the course of sleep in both age groups. The between-group difference in SWA diminished in the course of sleep, whereas the difference in activity in the frequency range of sleep spindles (12.25 – 14.0 Hz) increased. It is concluded that frequency and state specific changes occur as a function of age, and that the sleep dependent decline in SWA and increase in sleep spindle activity are attenuated with age.

Melatonin effect on daytime sleep in men: suppression of EEG low frequency activity and enhancement of spindle frequency activity

The effect of melatonin (5 mg, p.o.) on electroencephalographic (EEG) activity during sleep was investigated in eight men in a placebo-controlled cross-over design. Melatonin was administered immediately prior to a 4-h daytime sleep episode (13–17 h) after a partial sleep deprivation. The non-REM sleep stages and REM sleep duration were not significantly affected. Melatonin enhanced EEG power density in non-REM sleep in the 13.75–14.0 Hz bin (i.e., within the frequency range of sleep spindles), and reduced activity in the 15.25–16.5 Hz band. In the first 2 h spectral values within the 2.25–5.0 Hz range were reduced. These changes in the EEG are to some extent similar to those induced by benzodiazepine hypnotics and to the contribution of the endogenous circadian pacemaker to the spectral composition of the sleep EEG when sleep occurs at night.

EEG slow waves and sleep spindles: windows on the sleeping brain

Slow waves and sleep spindles are prominent features of the EEG in non-REM sleep and some of the neurophysiological mechanisms underlying their genesis have been elucidated. In humans, slow-wave activity in non-REM sleep increases and EEG activity in the frequency range of sleep spindles decreases when wakefulness prior to sleep is varied from 2 to 40 h. The opposite changes are observed in the course of sleep, even when sleep is scheduled out of phase with the circadian rhythm of sleep propensity. Within non-REM sleep episodes the association between slow waves and sleep spindles is bi-phasic: both activities are correlated positively at the beginning and end of non-REM sleep episodes whereas in the middle part of non-REM sleep episodes high values of slow-wave activity coincide with low levels of spindle activity. An extension of wakefulness enhances the rise rate of slow-wave and spindle activity at the onset of sleep. Since macroscopic slow waves and sleep spindles both are dependent on hyperpolarization and synchronization of neurons in thalamo-cortical and cortical circuits, the sleep deprivation induced changes in these EEG activities may be related to reduced activating input to thalamo-cortical and cortical neurons, local facilitation of their hyperpolarization or facilitation of their synchronization. The precise regulation of slow-wave and spindle activity as a function of the duration and intensity of prior sleep and wakefulness demonstrates that these EEG oscillations are accurate indicators of non-REM-sleep homeostatis and suggests that they are fundamental to the sleeping brain.

Caffeine intake (200 mg) in the morning affects human sleep and EEG power spectra at night

Adenosine has been implicated in the physiological regulation of sleep propensity. The adenosine-receptor-antagonist, caffeine (100 mg), administered immediately prior to a nocturnal sleep episode, has previously been shown to lower sleep propensity as indexed by a reduced sleep efficiency, a reduced EEG power density in low delta frequencies and enhanced power density in the frequency range of sleep spindles. To further investigate the role of adenosine in sleep regulation we administered 200 mg of caffeine at 07.10 h and analyzed the sleep stages and EEG power spectra during the subsequent night in nine healthy men. Caffeine levels in saliva decreased from a maximum of 17 μmol/l one hour after intake, to 3 μmol/l immediately prior to the sleep episode starting at 23.00 h. Compared to placebo, sleep efficiency and total sleep time were significantly reduced. EEG power density in nonREM sleep was suppressed in the 0.25–0.5 Hz band and enhanced in the frequency range of sleep spindles (11.25–12.0 Hz and 13.25–14.0 Hz). In REM sleep EEG power density was suppressed in the frequency range of 0.75–4.5 and 5.25–6.0 Hz. The data indicate that a saliva level of caffeine as low as 3 μmol/l directly affects sleep propensity or, alternatively, that the presence of caffeine in the central nervous system during the waking episode reduces the progressive increase of sleep propensity associated with wakefulness.

Cellular basis of EEG slow rhythms: a study of dynamic corticothalamic relationships

A slow oscillation (< 1 Hz) has recently been described in intracellular recordings from the neocortex and thalamus (Steriade et al., 1993c-e). The aim of the present study was to determine the phase relations between cortical and thalamic neuronal activities during the slow EEG oscillation. Intracellular recordings were performed in anesthetized cats from neurons in motor and somatosensory cortical areas, the rostrolateral sector of the reticular (RE) thalamic nucleus, and thalamocortical (TC) cells from ventrolateral (VL) nucleus. The EEG was used as time reference for alignment of activities in different, simultaneously recorded neurons, including dual impalements of cortical cells as well as cortical and TC cells. The spontaneous EEG oscillation was characterized by slowly recurring (0.3-0.9 Hz) sequences of surface-positive (depth-negative) sharp deflections, often followed by oscillatory activity within the frequency range of sleep spindles (7-14 Hz) or at faster frequencies. Cortical and RE cells were similarly hyperpolarized during the depth-positive EEG waves and were depolarized during the depth-negative EEG deflections. In many instances, the cell depolarization was associated with oscillations at the spindle frequency or with tonic firing at rates related to the level of depolarization. TC neurons were hyperpolarized during the depth-positive EEG waves and displayed a series of IPSPs, at the spindle frequencies, during the depth-negative EEG waves. Depending on the membrane potential (Vm), TC cells could fire spike bursts at the onset of the EEG depth-negativity, or their firing could be delayed by subsequent IPSPs. The sequence of spontaneous EEG and cellular events described above also characterized the responses to cortical and thalamic stimulation. Simultaneous intracellular recordings of pairs of cortical cells or cortical and TC cells showed that spontaneous transitions from less synchronized to more synchronized EEG states were marked by a simultaneous hyperpolarization, coincident with an overt depth-positive EEG wave. We conclude that during low-frequency oscillatory states, characteristic of slow-wave sleep, neocortical and thalamic neurons display phase relations that are restricted to narrow time windows, and that synchronization results from a generalized inhibitory phenomenon. Moreover, EEG synchronization is reflected as active inhibition in TC neurons. That this pattern is also present in states of hypersynchronization, such as seizure activity, is shown in the following paper (Steriade and Contreras, 1994).

All-night dynamics of the human sleep EEG.

The dynamics of the sleep EEG were investigated by all-night spectral analysis of 51 sleep records. Power density was calculated for 1-Hz bins in the 0.25-25.0 Hz range. Values in non-rapid-eye-movement sleep (NREMS) were higher than in REMS in the 0.25-16.0 Hz range, and lower in the 18.25-22.0 Hz range. Power density in the 0.25-12.0 Hz range showed a declining trend over the first four NREMS episodes, which, depending on the frequency bin, could be approximated by non-linear or linear decay functions. In the frequency range of sleep spindles (12.25-15.0 Hz), power density in the 13.25-15.0 Hz band showed an increasing trend between NREMS episode 2 and NREMS episode 4. A correlation matrix of 25 1-Hz bins revealed for NREMS a negative correlation between slow-wave activity (SWA; 0.25-4.0 Hz) and activity in the spindle frequency range. This negative correlation was highest in the first NREMS episode and diminished progressively over the subsequent NREMS episodes. Within NREMS episodes, the values in the spindle frequency range showed a U-shaped time course, the trough coinciding with a high level of SWA. By contrast, in both the early and late part of the episode the two types of activity changed in the same direction. The results are consistent with recent electrophysiological studies indicating that the establishment of NREMS is associated with a progressive hyperpolarization of thalamocortical neurons during which the membrane potential exhibits oscillations first in the spindle frequency range and then in the range of SWA.

A single dose of benzodiazepine hypnotics alters the sleep EEG in the subsequent drug-free night

All-night spectral analysis of the sleep EEG was used to study the effect and after-effect of a single bedtime dose of flunitrazepam (2 mg), flurazepam (30 mg) or triazolam (0.5 mg) in healthy young males. In the night of drug treatment all 3 hypnotics reduced the EEG slow waves and enhanced the activity in the frequency range of sleep spindles. In the subsequent drug-free night, the latter changes were no longer present after triazolam, whereas the reduction of slow wave activity persisted after all compounds.