Fronto-occipital EEG power gradients in human sleep

The brain topography of power spectra along the antero-posterior (A-P) axis was studied in the all-night human sleep EEG. Spectra (0.25–25.0 Hz) were computed for an anterior (A; F3-C3), a middle (M; C3-P3) and a posterior (P; P3-O1) bipolar derivation, and the spectral gradients between two adjacent derivations were expressed by power ratios (A/M and M/P). At NREM-REM sleep transitions a power shift from A to M was present over almost the entire frequency range, while the direction of shifts between M and P differed between frequency bands. Within NREM sleep, frequency specific power gradients were present: In the low delta band power in both A (0.25 Hz bin) and P (0.25–1.0 Hz bins) was higher than in M. In the 4–9 Hz range the relation was A>M>P, and in the 15–25 Hz range power was largest in M. Power in the spindle frequency range was highest at 11.75 Hz in M, and at 13.5–13.75 Hz in A. Topographical differences were seen also in the temporal changes of power across and within NREM sleep episodes. Whereas NREM sleep power in the 2-Hz bin was higher in A than in M in the first episode, this difference vanished in the course of the night. This result points to a specific involvement of frontal parts of the cortex in sleep homeostasis. The regional differences in sleep EEG spectra indicate that sleep is not only a global phenomenon but also a local brain process with a different regional involvement of neuronal populations.     

Regional differences in NREM sleep slow-wave activity in mice with congenital callosal dysgenesis

Topographic differences in the sleep EEG have been repeatedly found in humans and rodents. A frontal predominance of EEG slow-wave activity (0.75-4 Hz; delta band) during non-rapid eye movement (NREM) sleep is particularly evident under conditions of increased sleep propensity. Local aspects of neuronal connectivity in the neocortex that are modified by specific neuronal stimulation may underlie these differences. To investigate the role of altered neuronal connectivity on anterior-posterior EEG topography, sleep was recorded in mice with congenital dysgenesis of the corpus callosum (B1 strain) during baseline and after 6 h sleep deprivation (SD). In these mice neuronal connections within a hemisphere are increased due to the longitudinal Probst bundle, a structure of re-routed callosal fibers. After SD the frequencies above 1.5 Hz within the delta band in NREM sleep were reduced in B1 mice compared with control C57BL/6 mice, a strain that has a normal corpus callosum, while power in the lowest frequency band (0.75-1.0 Hz) was enhanced in B1 mice. The differences between the strains subsided in the course of recovery. The redistribution of EEG power within the delta band in the frontal region in mice with a well developed Probst bundle, suggests a role of intracortical connectivity in local sleep regulation.     

Age trends in the sleep EEG of healthy older men and women

SUMMARY  The all-night sleep EEGs of 314 (191 women, 123 men) healthy older subjects between the ages of 45 and 90 were studied for age trends in the power spectra of the all-night NREM sleep EEG. Power spectra of the unnormalized EEG of the women show a power loss in the delta band and a power increase in the beta band with increasing age. For the men no significant trends in the power spectra of the unnormalized EEG were in evidence. A normalization of the power spectra was performed by referencing each logarithmically expressed spectra to its area between 2 Hz and 30 Hz. For both genders the normalized spectra show significant decreases in power at many frequencies below 16 Hz and significant increases in power at frequencies above 18 Hz with increasing age. The age trends observed in the spectra of this population (45-90y age group) are about a third of the magnitude of those reported in the literature for subjects between the ages of 20y and 40y.     

Zolpidem and sleep deprivation: different effect on EEG power spectra

To study the role of GABA-ergic mechanisms in sleep regulation, the combined action of 40 h sleep deprivation and either 20 mg zolpidem or placebo on the sleep electroencephalogram (EEG) were investigated by quantitative EEG analysis in eight young men who participated in a positron emission tomography study. Compared with baseline, sleep deprivation increased low-frequency (1.25-7.0 Hz) EEG power in non-rapid eye movement (NREM) sleep in the placebo night. After administration of zolpidem, power in the 3.75-10.0 Hz range and 14. 25-16.0 Hz band was reduced. The largest decrease was observed in the theta band. Comparison with placebo revealed that zolpidem attenuated power in the entire 1.75-11.0 Hz range. The plasma concentration of zolpidem at 4.5 h after intake showed a positive correlation with the drug-induced difference in power from placebo in the 14.25-16.0 Hz band. Regional EEG analysis based on bipolar derivations along the antero-posterior axis disclosed, for NREM sleep, a drug-induced posterior shift of power in the frequency range of 7.75-9.75 Hz. Zolpidem did not affect rapid eye movemnt sleep spectra. We conclude that sleep deprivation and agonistic modulation of GABAA receptors have separate and additive effects on power spectra and that their effects are mediated by different neurophysiological mechanisms.     

Homeostatic behavior of fast Fourier transform power in very low frequency non-rapid eye movement human electroencephalogram

Basic research shows that the physiological and molecular mechanisms of very low frequency (<1 Hz) electroencephalogram (EEG) waves of non-rapid eye movement (NREM) sleep differ from those of the higher (1–4 Hz) delta frequencies. Human studies show that the across-NREM period dynamics of very low frequency and 1–4 Hz EEG also differ. These differences and the reported failure of very low frequency EEG power to increase after a night of total sleep deprivation raise the question of whether very low frequency EEG shows the other homeostatic properties established for higher delta frequencies. Here we tested the relation of very low frequency EEG power density to prior waking duration across a normal day and whether these low frequencies meet another criterion for homeostatic sleep EEG: conservation of power across a late nap and post-nap sleep. Data from 19 young adults recorded in four separate sessions of baseline, daytime nap and post-nap sleep were analyzed. Power density in very low frequency NREM EEG increased linearly when naps were taken later in the day (i.e. were preceded by longer waking durations). In the night following an 18:00 h nap, very low frequency power was reduced by roughly the amount of power in the nap. Thus, very low frequency EEG meets two major homeostatic criteria. We hypothesize that these low frequencies reflect the executive rather than the functional processes by which NREM sleep reverses the effects of waking brain activity.     

Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence

We examined the sleep electroencephalogram (EEG) in 9- and 10-year-old children with (PH+) and without (PH−) a parental history of alcohol abuse/dependence to determine whether sleep disturbances associated with alcohol precede the onset of alcohol use. Participants slept on a fixed sleep schedule that ensured at least a 10-h time in bed for 1 week before an adaptation and baseline night. Data were collected in a four-bed sleep research laboratory. Thirty healthy boys and girls aged 9 or 10 years were classified as either PH+ or PH− based on DSM-IV criteria applied to structured parental interviews. All-night polysomnography was performed, sleep data were scored visually in 30-s epochs, and EEG power spectra were calculated for each epoch. All-night EEG spectra were calculated for rapid eye movement (REM) and non-REM (NREM) sleep, and cycle-by-cycle spectra were calculated for NREM sleep. The two groups did not differ on any sleep stage variable. All-night analyses revealed normalized power in the delta band and spindle range were lower in PH+ children. Within NREM sleep cycles PH+ children exhibited less normalized power in the delta band and spindle range compared with PH− children. This effect occurred in the first four cycles and was most pronounced in the first sleep cycle of the night. We found no signs of sleep disruption in sleep stages for PH+ children. Sleep EEG spectral differences, however, suggest that certain circuits responsible for 'protecting' sleep may be impaired in PH+ children, which may lead to disrupted sleep later in life.     

The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

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.     

Spectral analysis of all-night human sleep EEG in narcoleptic patients and normal subjects

To investigate the pathophysiology of narcoleptic patients' sleep in detail, we analysed and compared the whole-night polysomnograms of narcoleptic patients and normal human subjects. Eight drug-naive narcoleptic patients and eight age-matched normal volunteers underwent polysomnography (PSG) on two consecutive nights. In addition to conventional visual scoring of the polysomnograms, rapid eye movement (REM)-density and electroencephalograph (EEG) power spectra analyses were also performed. Sleep onset REM periods and fragmented nocturnal sleep were observed as expected in our narcoleptic patients. In the narcoleptic patients, REM period duration across the night did not show the significant increasing trend that is usually observed in normal subjects. In all narcoleptic patient REM periods, eye movement densities were significantly increased. The power spectra of narcoleptic REM sleep significantly increased between 0.3 and 0.9 Hz and decreased between 1.0 and 5.4 Hz. Further analysis revealed that non-rapid eye movement (NREM) period duration and the declining trend of delta power density in the narcoleptic patients were not significantly different from the normal subjects. Compared with normal subjects, the power spectra of narcoleptic NREM sleep increased in the 1.0-1.4 Hz and 11.0-11.9 Hz frequency bands, and decreased in a 24.0-26.9 Hz frequency band. Thus, increased EEG delta and decreased beta power densities were commonly observed in both the NREM and REM sleep of the narcoleptic patients, although the decrease in beta power during REM sleep was not statistically significant. Our visual analysis revealed fragmented nocturnal sleep and increased phasic REM components in the narcoleptic patients, which suggest the disturbance of sleep maintenance mechanism(s) and excessive effects of the mechanism(s) underlying eye movement activities during REM sleep in narcolepsy. Spectral analysis revealed significant increases in delta components and decreases in beta components, which suggest decreased activity in central arousal mechanisms. These characteristics lead us to hypothesize that two countervailing mechanisms underlie narcoleptic sleep pathology.     

Comparison of MK-801 and sleep deprivation effects on NREM, REM, and waking spectra in the rat.

In previous studies, we showed that blockade of the cation channel gated by NMDA glutamate receptors with ketamine or MK-801 massively stimulates NREM delta. We now test whether this NREM delta stimulation is physiological by comparing the EEG response following MK-801 to the EEG response following sleep deprivation (SD). Our previous studies measured only NREM 1-4 Hz EEG with period-amplitude analysis (PAA). Here we extended the analysis of MK-801 effects on sleep EEG by applying power spectral analysis (PSA) to examine delta and higher frequency spectra (.2-100 Hz) in NREM and by including REM and waking spectra. The changes in EEG spectra following MK-801 and SD were remarkably similar. Both SD and MK-801 produced their largest changes in NREM delta and REM 10-20 Hz power. There were some differences in the high frequency EEG, but the overall similarity of the PSA spectra in all three vigilance states after MK-801 and SD supports the possibility that MK-801 stimulated physiologic sleep, perhaps by increasing the need for homeostatic recovery from the metabolic effects of NMDA channel blockade.     

Developmental changes in the sleep electroencephalogram of adolescent boys and girls

The sleep electroencephalogram (EEG) changes across adolescence; however, there are conflicting data as to whether EEG changes are regionally specific, are evident in non‐rapid eye movement (NREM) and rapid eye movement (REM) sleep, and whether there are sex differences. The present study seeks to resolve some of these issues in a combined cross‐sectional and longitudinal analysis of sleep EEG in adolescents. Thirty‐three healthy adolescents (18 boys, 15 girls; 11–14 years) were studied on two occasions 6–8 months apart. Cross‐sectional analysis of data from the initial visit revealed significantly less slow‐wave sleep, delta (0.3 to <4 Hz) and theta (4 to <8 Hz) power in both NREM and REM sleep with advancing age. The age–delta power relationship was significant at the occipital site, with age accounting for 26% of the variance. Longitudinal analysis revealed that NREM delta power declined significantly from the initial to follow‐up visit, in association with declining delta amplitude and incidence (P < 0.01), with the effect being greatest at the occipital site. REM delta power also declined over time in association with reduced amplitude (P < 0.01). There were longitudinal reductions in theta, alpha and sigma power in NREM and REM sleep evident at the occipital site at follow‐up (P < 0.01). No sex differences were apparent in the pattern of change with age for NREM or REM sleep. Declines in sleep EEG spectral power occur across adolescence in both boys and girls, particularly in the occipital derivation, and are not state‐specific, occurring in both NREM and REM sleep.     

Sleep and EEG spectra in the rabbit under baseline conditions and following sleep deprivation

The 24-hr sleep-wake distribution and power spectra of the electroencephalogram were determined in rabbits that had been implanted with cortical and hippocampal electrodes. A diurnal preference for sleep was observed. The spectral power density in nonrapid eye movement sleep (NREM sleep) of the cortex showed a decreasing trend in most frequencies within the 12-hr light period. In the 12-hr dim period no clear trend was present. Most hippocampal EEG frequencies decreased in NREM sleep in the first two hours of the light period, and thereafter stayed on a constant level. Sleep deprivation elicited the following changes: a prolonged increase of NREM sleep and a short increase of REM sleep; in the cortex, an increase of slow-wave activity (SWA; power density in the 0.25-2.0 Hz frequency band) in NREM sleep, which declined in the course of recovery; an enhancement of slow-wave (1.25-3 Hz) and theta (6.25-7 Hz) activity in REM sleep. The hippocampus showed an increase in NREM sleep power density in almost all frequencies. In REM sleep the hippocampus exhibited an increase in power density in the 6.25-7 Hz and 12.25-13 Hz bands, whereas in the 7.25-8 Hz band the values were below baseline. The results show that SWA in NREM sleep and theta activity in REM sleep are enhanced by sleep deprivation, as has been observed in other mammalian species. The EEG changes in the hippocampus resembled those in the cortex.     

All night spectral analysis of EEG sleep in young adult and middle-aged male subjects

The sleep EEGs of 9 young adult males (age 20–28 years) and 8 middle-aged males (42–56 years) were analyzed by visual scoring and spectral analysis. In the middle-aged subjects power density in the delta, theta and sigma frequencies were attenuated as compared to the young subjects. In both age groups power density in the delta and theta frequencies declined from NREM period 1 to 3. In the sigma frequencies, however, no systematic changes in power density were observed over the sleep episode. In both age groups the decay of EEG power (0.75–7.0 Hz) over successive NREM-REM cycles and the time course of EEG power during NREM sleep was analyzed. The decay rate of both EEG power density over successive NREM-REM cycles and EEG power density during NREM sleep was smaller in the middle-aged subjects than in the young subjects. It is concluded that the age-related differences in human sleep EEG power spectra are not identical to the changes in EEG power spectra observed in the course of the sleep episode. Therefore age-related differences in EEG power spectra cannot be completely explained by assuming a reduced need for sleep in older subjects. The smaller decay rate of EEG power during NREM sleep in the middle-aged subjects is interpreted as a reduced sleep efficiency. The results are discussed in the frame work of the two-process model of sleep regulation.     

Changes in EEG power density of NREM sleep in depressed patients during treatment with citalopram

According to a recent hypothesis the therapeutic effects of antidepressants might be related to acute or cumulative suppression of NREM sleep intensity. This intensity has been proposed to be expressed in the EEG power density in NREM sleep. In the present study the relationship was examined between the changes of EEG power density in NREM sleep and the changes in clinical state in 16 depressed patients during treatment with citalopram, a highly specific serotonin uptake inhibitor. A one-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a one-week placebo period. In order to minimize systematic influences of sleep duration and NREM-REM sleep alterations, EEG power was measured over the longest common amount of NREM sleep stages 2, 3 and 4 (91.5 min). During the last treatment week and the week after withdrawal, a significant decrease of EEG power as compared to baseline was found in the 8-9 Hz frequency range. No clear-cut change, however, was observed in the EEG power of the delta frequency range (1-4 Hz), which is considered to be the principle manifestation of NREMS intensity. Furthermore, no relationship between changes in EEG power density and changes in clinical state could be demonstrated.     

Effects of eszopiclone and zolpidem on sleep and waking states in the adult guinea pig

STUDY OBJECTIVE: The present study was designed to compare and contrast the effects of eszopiclone and zolpidem on the states of sleep and wakefulness in chronically instrumented, unanesthetized adult guinea pigs. DESIGN: Adult guinea pigs were implanted with electrodes to record sleep and waking states and to perform a frequency analysis of the EEG. Eszopiclone (1 and 3 mg/kg) and zolpidem (1 and 3 mg/kg) were administered intraperitoneally. MEASUREMENTS AND RESULTS: The administration of eszopiclone (1 and 3 mg/kg) resulted in a significant dose-dependent increase in NREM sleep. Zolpidem produced a significant increase in NREM sleep, but only at a dose of 3 mg/kg. The following changes in NREM and REM sleep, as well as in the power spectra, were all significant when the effects of 1 and 3 mg/kg of eszopiclone were compared with responses induced with 1 and 3 mg/kg of zolpidem, respectively: The increase in NREM sleep produced by eszopiclone was greater than that following the administration of zolpidem. The mean latency to NREM sleep following the administration of eszopiclone was significantly shorter than zolpidem. Eszopiclone significantly increased the latency to REM sleep. The mean duration of episodes of NREM sleep was increased by eszopiclone, but not by zolpidem. The EEG power increased in the delta band and decreased in the theta band during NREM sleep following the administration of eszopiclone. No significant changes occurred in any of the frequency bands analyzed following zolpidem administration. CONCLUSIONS: The differences in the effects of eszopiclone and zolpidem on sleep and waking states and the power spectra of the EEG likely reflect the fact that eszopiclone and zolpidem bind to different subunits of the GABAA receptor complex.     

EEG Spectral Analysis in Primary Insomnia: NREM Period Effects and Sex Differences

Study Objectives:

To compare NREM EEG power in primary insomnia (PI) and good sleeper controls (GSC), examining both sex and NREM period effects; to examine relationships between EEG power, clinical characteristics, and self-reports of sleep.

Design:

Overnight polysomnographic study.

Setting:

Sleep laboratory.

Participants:

PI (n = 48; 29 women) and GSC (n = 25; 15 women).

Interventions:

None.

Measurements:

EEG power from 1–50 Hz was computed for artifactfree sleep epochs across four NREM periods. Repeated measures mixed effect models contrasted differences between groups, EEG frequency bands, and NREM periods. EEG power-frequency curves were modeled using regressions with fixed knot splines.

Results:

Mixed models showed no significant group (PI vs. GSC) differences; marginal sex differences (delta and theta bands); significant differences across NREM periods; and group*sex and group*NREM period interactions, particularly in beta and gamma bands. Modeled power-frequency curves showed no group difference in whole-night NREM, but PI had higher power than GSC from 18–40 Hz in the first NREM period. Among women, PI had higher 16 to 44-Hz power than GSC in the first 3 NREM periods, and higher 3 to 5-Hz power across all NREM periods. PI and GSC men showed no consistent differences in EEG power. High-frequency EEG power was not related to clinical or subjective sleep ratings in PI.

Conclusions:

Women with PI, but not men, showed increased high-frequency and low-frequency EEG activity during NREM sleep compared to GSC, particularly in early NREM periods. Sex and NREM period may moderate quantitative EEG differences between PI and GSC.

Citation:

Buysse DJ; Germain A; Hall ML; Moul DE; Nofzinger EA; Begley A; Ehlers CL; Thompson W; Kupfer DJ. EEG spectral analysis in primary insomnia: NREM period effects and sex differences. SLEEP 2008;31(12):1673–1682.     

Cholinergic regulation of the central nucleus of the amygdala in rats: effects of local microinjections of cholinomimetics and cholinergic antagonists on arousal and sleep

The amygdala has emerged as an important forebrain modulator of arousal. Acetylcholine plays a role in the regulation of sleep and wakefulness, particularly rapid eye movement sleep (REM). The major cholinergic input to the amygdala comes from the basal forebrain, a region primarily linked to wakefulness. We examined sleep and the encephalogram for 8 h following bilateral microinjections into the central nucleus of the amygdala (CNA) of the cholinergic agonist, carbachol (CARB(L): 0.3 microg; CARB(H): 3.0 microg), the acetylcholinesterase inhibitor, neostigmine (NEO(L): 0.3 microg; NEO(H): 3.0 microg), the muscarinic antagonist, scopolamine (SCO(L): 0.3 microg; SCO(H): 1.0 microg), the nicotinic antagonist, mecamylamine (MEC(L): 0.3 microg; MEC(H): 1.0 microg) and saline (SAL, 0.2 microl) alone. Both doses of CARB and NEO significantly reduced REM, but did not significantly alter non-rapid eye movement sleep (NREM). Both doses of SCO significantly increased NREM, and SCO(H) also produced an initial increase in REM followed by a significant decrease. CARB(H) and NEO(H) decreased REM electroencephalogram (EEG) power in the 5.5-10 Hz band, and NEO(L) and NEO(H) decreased NREM EEG power in the 0.5-5.0 Hz band. CARB(L) decreased waking EEG power in the 0.5-5.0 Hz band, and NEO(H) decreased waking EEG power in the 5.0-10.0 Hz band. Both doses of SCO significantly increased waking EEG power in the 5.5-10.0 Hz band. Compared with SAL, MEC did not significantly alter sleep or EEG power. The reduction of REM by CARB and NEO and the alteration of sleep by SCO indicate that cholinergic regulation of the amygdala is involved in the control of arousal in rodents. In contrast, CARB microinjections into CNA increase REM in cats, though the reasons for the species difference are not known. The results are discussed in the context of anatomical inputs and species differences in the cholinergic regulation of CNA.     

Sex differences in brain oscillatory activity during sleep and wakefulness in obstructive sleep apnea

Epidemiological studies consistently show a male predominance in obstructive sleep apnea (OSA). Hormonal differences, breathing control, upper airway anatomy and fat distribution have been proposed as causes of gender differences in OSA. Clinical manifestations are accentuated in men, although white matter structural integrity is affected in women. To the best of our knowledge, no previous studies have explored gender differences in the electrical brain activity features of OSA. Polysomnography was performed on 43 patients with untreated OSA (21 women, 22 men), and power spectral density (1–50 Hz) was compared between groups across sleep and wakefulness at two levels of OSA severity. Severe versus moderate OSA showed decreased power for fast frequencies (25–29 Hz) during wakefulness. OSA men displayed decreased power of a large frequency range (sigma, beta and gamma) during sleep compared with women. Comparisons of men with severe versus moderate OSA presented significantly decreased sigma power during non‐rapid eye movement (NREM) sleep, but significantly increased delta activity during REM sleep. Meanwhile, women with severe versus moderate OSA showed no significant power differences in any condition. These findings indicated a different evolution of brain oscillations between OSA men and women with significant impairment of brain activity related to cognitive processes. Our study emphasizes the importance of understanding the differential effects of sleep disorders on men and women in order to develop more precise diagnostic criteria according to gender, including quantitative electroencephalogram (EEG) analysis tools.     

Age effects on spectral electroencephalogram activity prior to dream recall

Ageing is associated with marked changes in sleep timing, structure and electroencephalographic (EEG) activity. Older people exhibit less slow-wave and spindle activity during non-rapid eye movement (NREM) sleep, together with attenuated levels of rapid eye movement (REM) sleep as compared to young individuals. However, the extent to which these age-related changes in sleep impact on dream processing remains largely unknown. Here we investigated NREM and REM sleep EEG activity prior to dream recall and no recall in 17 young (20-31 years) and 15 older volunteers (57-74 years) during a 40 h multiple nap protocol. Dream recall was assessed immediately after each nap. During NREM sleep prior to dream recall, older participants displayed higher frontal EEG delta activity (1-3 Hz) and higher centro-parietal sigma activity (12-15 Hz) than the young volunteers. Conversely, before no recall, older participants had less frontal-central delta activity and less sigma activity in frontal, central and parietal derivations than the young participants. REM sleep was associated to age-related changes, such that older participants had less frontal-central alpha (10-12 Hz) and beta (16-19 Hz) activity, irrespective of dream recall and no recall. Our data indicate that age-related differences in dream recall seem to be directly coupled to specific frequency and topography EEG patterns, particularly during NREM sleep. Thus, the spectral correlates of dreaming can help to understand the cortical pathways of dreaming.     

Effects of sleep restriction on the sleep electroencephalogram of adolescents

Study ObjectivesThis report describes findings from an ongoing longitudinal study of the effects of varied sleep durations on wake and sleep electroencephalogram (EEG) and daytime function in adolescents. Here, we focus on the effects of age and time in bed (TIB) on total sleep time (TST) and nonrapid eye movement (NREM) and rapid eye movement (REM) EEG.MethodsWe studied 77 participants (41 male) ranging in age from 9.9 to 16.2 years over the 3 years of this study. Each year, participants adhered to each of three different sleep schedules: four consecutive nights of 7, 8.5, or 10 h TIB.ResultsAltering TIB successfully modified TST, which averaged 406, 472 and 530 min on the fourth night of 7, 8.5, and 10 h TIB, respectively. As predicted by homeostatic models, shorter sleep durations produced higher delta power in both NREM and REM although these effects were small. Restricted sleep more substantially reduced alpha power in both NREM and REM sleep. In NREM but not REM sleep, sleep restriction strongly reduced both the all-night accumulation of sigma EEG activity (11–15 Hz energy) and the rate of sigma production (11–15 Hz power).ConclusionsThe EEG changes in response to TIB reduction are evidence of insufficient sleep recovery. The decrease in sigma activity presumably reflects depressed sleep spindle activity and suggests a manner by which sleep restriction reduces waking cognitive function in adolescents. Our results thus far demonstrate that relatively modest TIB manipulations provide a useful tool for investigating adolescent sleep biology.