Psychological stress is associated with heightened physiological arousal during NREM sleep in primary insomnia

The objective of this study was to evaluate cross-sectional relationships among symptoms of psychological stress, sleep, and physiological arousal during non-rapid eye movement (NREM) sleep in a sample of 30 patients with chronic, primary insomnia (mean age, 30.2 years, 60% female). Study measures included indexes of subjective stress, visually scored sleep, and physiological arousal during NREM sleep: quantitative electroencephalogram (QEEG) and quantitative electrocardiogram (QEKG) measures. Psychological stress was more strongly related to indexes of physiological arousal during NREM sleep than to visually scored measures of sleep. Higher levels of perceived stress were associated with decreased EEG delta power (rho = -0.50, p < .01) and increased EEG beta power (rho = 0.38, p < .05). Increased frequency of stress-related avoidance behaviors was associated with decreased EKG high-frequency power (rho = -0.46, p < .05). Although QEEG measures were significantly correlated with sleep maintenance (QEEG delta power rho = 0.45, p < .01; QEEG beta power rho = -0.54, p < .01) and time spent in delta sleep (QEEG delta power rho = 0.65, p < .001; QEEG beta power rho = -0.65, p < .001), QEKG measures were unrelated to visually scored measures of sleep. Perceived stress and stress-related avoidance behaviors were associated with multiple indexes of physiological arousal during NREM sleep in patients with chronic, primary insomnia.     

Beta/Gamma EEG activity in patients with primary and secondary insomnia and good sleeper controls

STUDY OBJECTIVE: Several studies have shown that patients with insomnia exhibit elevated levels of Beta EEG activity (14-35 Hz) at or around sleep onset and during NREM sleep. In this study, we evaluated 1) the extent to which high frequency EEG activity is limited to the 14-32 Hz domain, 2) whether high frequency EEG activity (HFA) is associated with discrepancies between subjective and PSG measures of sleep continuity, and 3) the extent to which high frequency EEG activity occurs in patients with primary, as opposed to secondary, insomnia. DESIGN: Three groups (n=9 per group) were compared: Primary Insomnia, Insomnia secondary to Major Depression, and Good Sleeper Controls. Groups were matched for age, sex and body mass. Average spectral profiles were created for each NREM cycle after removing waking and movement epochs and epochs containing micro- or mini-arousals. SETTING: Sleep Research Laboratory PATIENTS OR PARTICIPANTS: Patients with primary and secondary insomnia INTERVENTIONS: N/A MEASUREMENTS AND RESULTS: Subjects with Primary Insomnia exhibited more average NREM activity for Beta-1 (14-20Hz), Beta-2 (20-35Hz) and Gamma activity (35-45Hz) than the other two groups (p.<.01). Group differences were also suggestive for Omega activity (45.0-125Hz) (p.<.10), with MDD subjects tending to exhibit more activity than the other groups. Correlational analyses revealed that average NREM Beta-1 and Beta-2 activity tended to be negatively correlated with subjective-objective discrepancy measures for total sleep time and sleep latency. CONCLUSIONS: Our results confirm that Beta activity is increased in Primary Insomnia. In addition, our data suggest that high frequency activity in patients with Primary Insomnia is limited to the Beta/Gamma range (14-45 Hz), and is negatively associated with the perception of sleep.     

Sex differences in delta and alpha EEG activities in healthy older adults

STUDY OBJECTIVES: To examine sex effects on sleep stages and electroencephalogram (EEG) spectral power in older adults. DESIGN: Sleep was polygraphically recorded for 2 consecutive nights, and blood was sampled during the last 24 hours. SETTING: The University of Chicago Clinical Research Center. PARTICIPANTS: Two groups of healthy nonobese older subjects: 10 men (59 +/- 2 years), and 10 postmenopausal women (63 +/- 2 years). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: A spectral analysis of the EEG was performed in the delta and alpha bands. There were no sex differences in sleep stages. Blood sampling resulted in reductions of total sleep time, sleep maintenance, slow-wave sleep, and absolute delta activity that were all larger in women than in men. In absolute values, delta and alpha activities in non-rapid eye movement (NREM) and rapid eye movement (REM) sleep were higher in women than in men, but, for delta activity, the sex differences were larger in REM than in NREM sleep. In women, but not in men, absolute delta activity in REM was decreased during blood sampling and was strongly correlated with absolute delta activity in NREM. Delta activity in REM did not dissipate across the night in either group. When normalized for the activity in REM sleep, the sex difference in delta activity in NREM sleep was reversed, with lower activity in women. CONCLUSIONS: Sex differences in sleep EEG variables are present in older adults. When normalized, delta activity in older women is lower than in older men, which may be more consistent with sex differences in subjective complaints, in fragility of sleep in the presence of environmental disturbances, and in the relationship to growth-hormone release.     

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.     

Does REM sleep contribute to subjective wake time in primary insomnia? A comparison of polysomnographic and subjective sleep in 100 patients

Primary insomnia (PI) is characterized by low subjective sleep quality which cannot always be verified using polysomnography (PSG). To shed light on this discrepancy, subjective estimates of sleep and PSG variables were compared in patients with PI and good sleeper controls (GSC). 100 patients with PI (age: 42.57 +/- 12.50 years, medication free for at least 14 days) and 100 GSC (41.12 +/- 13.99 years) with a sex distribution of 46 men and 54 women in each group were included. Both PSG and questionnaire variables showed clear impairments of sleep quality in PI compared with GSC. The arousal index within total sleep time was increased, which was mainly because of a strong increase within rapid eye movement (REM) sleep. Subjectively, more PI than GSC subjects estimated wake times longer than obtained from PSG. Linear modeling analysis of subjective wake time in terms of PSG parameters revealed that in addition to PSG defined wake time, REM sleep time contributed significantly to subjective wake time. This REM sleep contribution was larger for PI than for GSC subjects. The findings suggest that REM sleep-related processes might contribute to subjectively disturbed sleep and the perception of waking time in patients with PI.     

Increased EEG sigma and beta power during NREM sleep in primary insomnia

The hyperarousal model of primary insomnia suggests that a deficit of attenuating arousal during sleep might cause the experience of non-restorative sleep. In the current study, we examined EEG spectral power values for standard frequency bands as indices of cortical arousal and sleep protecting mechanisms during sleep in 25 patients with primary insomnia and 29 good sleeper controls. Patients with primary insomnia demonstrated significantly elevated spectral power values in the EEG beta and sigma frequency band during NREM stage 2 sleep. No differences were observed in other frequency bands or during REM sleep. Based on prior studies suggesting that EEG beta activity represents a marker of cortical arousal and EEG sleep spindle (sigma) activity is an index of sleep protective mechanisms, our findings may provide further evidence for the concept that a simultaneous activation of wake-promoting and sleep-protecting neural activity patterns contributes to the experience of non-restorative sleep in primary insomnia.     

Increased EEG sigma and beta power during NREM sleep in primary insomnia

The hyperarousal model of primary insomnia suggests that a deficit of attenuating arousal during sleep might cause the experience of non-restorative sleep. In the current study, we examined EEG spectral power values for standard frequency bands as indices of cortical arousal and sleep protecting mechanisms during sleep in 25 patients with primary insomnia and 29 good sleeper controls. Patients with primary insomnia demonstrated significantly elevated spectral power values in the EEG beta and sigma frequency band during NREM stage 2 sleep. No differences were observed in other frequency bands or during REM sleep. Based on prior studies suggesting that EEG beta activity represents a marker of cortical arousal and EEG sleep spindle (sigma) activity is an index of sleep protective mechanisms, our findings may provide further evidence for the concept that a simultaneous activation of wake-promoting and sleep-protecting neural activity patterns contributes to the experience of non-restorative sleep in primary insomnia.     

Cortical activation patterns herald successful dream recall after NREM and REM sleep

Dreaming pertains to both REM and NREM sleep. However, frequency and regional specific differences in EEG activity remains controversial. We investigated NREM and REM sleep EEG power density associated with and without dream recall in 17 young subjects during a 40-h multiple nap protocol under constant routine conditions. NREM sleep was associated with lower EEG power density for dream recall in the delta range, particularly in frontal derivations, and in the spindle range in centro-parietal derivations. REM sleep was associated with low frontal alpha activity and with high alpha and beta activity in occipital derivations. Our data indicate that specific EEG frequency- and topography changes underlie differences between dream recall and no recall after both NREM and REM sleep awakening. This dual NREM-REM sleep modulation holds strong implications for the mechanistic understanding of this complex ongoing cognitive process.     

REM and NREM power spectral analysis on two consecutive nights in psychophysiological and paradoxical insomnia sufferers

The objectives of the study were to examine EEG activities using power spectral analysis (PSA) of good sleepers (GS), psychophysiological (PsyI) and paradoxical (ParI) insomnia sufferers on two consecutive nights. Participants completed three nights of PSG recordings in a sleep laboratory following a clinical evaluation. Participants were 26 PsyI, 20 ParI and 21 GS (mean age = 40 years, SD = 9.4). All sleep cycles of Nights 2 and 3 were retained for PSA. The absolute and relative activity in frequency bands (0.00 to 125.00 Hz) were computed at multiple frontal, central and parietal sites in REM and NREM sleep. Mixed model ANOVAs were performed with absolute and relative PSA data to assess differences between groups and nights. Over the course of the two nights, more absolute delta activity at F3, C3, and P3 was observed in ParI compared with PsyI suggesting deactivation of the left hemisphere in ParI and/or hyperactivation in PsyI. Further analysis on absolute PSA data revealed that differences between groups relate mostly to NREM. In REM, lower relative activity in slower frequency bands was found in ParI in comparison with GS and less relative theta activity was found in PsyI compared with GS implying higher activation in insomnia. In addition, between nights variability has been found in absolute powers of faster frequency bands (beta to omega). Signs of decreased cortical activity in absolute PSA in NREM combined with increased relative cortical activation in REM were found in ParI which might contribute to the misperception of sleep in ParI.     

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.     

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.     

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.     

Cardiac autonomic regulation during sleep in idiopathic REM sleep behavior disorder

OBJECTIVE: To assess cardiac autonomic and respiratory changes from stage 2 non-rapid eye movement sleep (NREM) to rapid eye movement (REM) sleep in subjects with idiopathic REM sleep behavior disorder (RBD) and controls. We tested the hypothesis that REM-related cardiorespiratory activation is altered in subjects with RBD. DESIGN: Retrospective case-control study. SETTING: University hospital-based sleep research laboratory. PATIENTS: Ten subjects with idiopathic RBD (2 women, mean age 63.4 +/- 6.2 years) and 10 sex- and age-matched controls (mean age 63.9 +/- 6.3 years). INTERVENTION: One-night polysomnography was used to assess R-R variability during NREM and REM sleep. MEASUREMENTS AND RESULTS: Spectral analysis of R-R interval and respiration were performed. Mean R-R interval, low-frequency (LF) and high-frequency (HF) components in both absolute and normalized units (LFnu and HFnu), and the LF/HF ratio were obtained from 5-minute electrocardiogram segments selected during NREM and REM sleep under stable conditions (stable breathing pattern, no microarousals or leg movements). Respiratory frequency was also assessed. Values obtained were then averaged for each stage and analyzed by 2 x 2 analysis of variance with group (RBD subjects and controls) as factor and state (NREM and REM) as repeated measures. RR interval, HF, and HFnu components decreased from NREM to REM in controls but did not change in RBD subjects (Interaction P < 0.05). LFnu (interaction P < 0. 001), LF/HF (interaction P < 0. 001), and respiratory frequency (interaction P < 0. 05) increased from NREM to REM sleep in controls but remained stable in RBD subjects. CONCLUSION: REM-related cardiac and respiratory responses are absent in subjects with idiopathic RBD.     

Psychophysiological insomnia: the behavioural model and a neurocognitive perspective

A number of paradoxes are apparent in the assessment and treatment of psychophysiological insomnia and sleep state misperception. Three of these paradoxes exist as discrepancies between polysomnographic (PSG) measures and the subjective impressions regarding sleep quality and quantity. The remaining incongruity exists largely within the objective domain. In the case of subjective–objective discrepancies, patients with insomnia: (1) frequently identify themselves as having been awake when awakened from PSG defined sleep; (2) tend to overestimate sleep latency and underestimate total sleep time as compared with PSG measures; (3) appear to derive more benefit from pharmacotherapy that can be explained by objective gains. The remaining paradox pertains to the observation that hypnotic medications, by and large, do not normalize sleep architecture or produce a more ‘sleep-like’ EEG. In this paper, we review possible explanations for these various paradoxes, introduce a new perspective and suggest possible research avenues. The model introduced is based on the observation that beta and/or gamma activity (which have been found to be associated with cognitive processes) is enhanced in insomnia at or around sleep onset. We propose that this kind of high frequency EEG activity may interfere with the normal establishment of sleep onset-related mesograde amnesia. As a result, the patient with insomnia maintains a level of information and/or memory processing that blurs the phenomenological distinction between sleep and wakefulness and influences retrospective judgments about sleep initiation and duration.     

Psychomotor performance deficits and their relation to prior nights' sleep among individuals with primary insomnia

OBJECTIVE: To examine psychomotor (reaction time) performance deficits and their relation to subjective and objective sleep measures among individuals with primary insomnia (PI). DESIGN AND SETTING: This study was conducted at affiliated VA and academic medical centers using a matched-groups, cross-sectional research design. PARTICIPANTS: Seventy-nine (43 women) individuals with PI (MAge = 50.0 +/- 17.1 y) and 84 (41 women) well-screened normal sleepers (MAge = 48.6 +/- 16.8 y). METHODS AND MEASURES: Participants underwent 3 nights of polysomnography (PSG) followed by daytime testing with a 4-trial multiple sleep latency test (MSLT). Before each MSLT nap, they rated their sleepiness and completed a performance battery that included simple reaction time (SRT), continuous performance (CPT), and 4 switching attention (SAT) tests. Performance measures included the mean response latency and the standard deviation of each subject's within-test response latencies. RESULTS: PI sufferers reported greater (P = 0.001) daytime sleepiness, but were significantly (P = 0.02), more alert than normal sleepers on the MSLT. Multivariate analyses showed the PI group had significantly longer response latencies and greater response variability across many of the subtests than did the controls. Regression analyses showed that both PSG- and diary-based sleep measures contributed to the prediction of daytime performance indices, although objective wake time after sleep onset appeared the best single predictor of the daytime measures. CONCLUSIONS: Results confirm that PI sufferers do show relative psychomotor performance deficits when responding to challenging reaction time tasks, and these deficits appear related to both objective and subjective sleep deficits. Findings support PI patients' diurnal complaints and suggest the usefulness of complex reaction time tasks for assessing them.     

Polysomnography findings in patients with restless legs syndrome and in healthy controls: a comparative observational study

STUDY OBJECTIVES: Sleep disturbances and their sequelae are the most common complaints of patients with restless legs syndrome (RLS). We compared polysomnography (PSG) findings in a large cohort of patients with idiopathic RLS and of healthy subjects. DESIGN: Comparative observational study. SETTING: University hospital sleep laboratory. PATIENTS: Age- and sex-matched patients with idiopathic but untreated RLS versus healthy controls. INTERVENTIONS: N/A RESULTS: Each group consisted of 29 females and 16 males. RLS subjects and controls were 47.4 +/- 10.9 and 47.3 +/- 10.5 years old, respectively. RLS severity was 24.0 +/- 6.2 points on the IRLS scale, indicating moderately severe RLS symptoms. We found strong multivariate group effects on PSG parameters (Wilks' lambda, P <0.001): RLS patients exhibited prolonged sleep onset latencies (according to the 10-min criterion but not to the one-epoch criterion), shorter total sleep time, lower sleep efficiency, higher arousal index, higher number of stage shifts, and longer REM sleep latency. During the sleep period time, percentage of wake and sleep stage 1 were increased, and sleep stage 2 and REM sleep were decreased in RLS patients. The PLMS indices and the sleep fragmentation index were markedly increased in the RLS group. CONCLUSIONS: We present the largest polysomnography study to date that compares patients with idiopathic RLS with age- and sex-matched healthy subjects. The findings demonstrate markedly fragmented sleep with deterioration of both NREM and REM sleep in RLS patients.     

Respiratory and body movements as indicators of sleep stage and wakefulness in infants and young children

Conventional polysomnographic (PSG) sleep staging to sleep staging based on a static-charge-sensitive bed (SCSB) recording in infants and young children was compared. The study consisted of whole-night clinical sleep studies in 22 children at 24 weeks (SD 24, range 1–79 weeks) of age. Most of the children presented with respiratory disturbances during sleep. From the SCSB record, sleep stages were differentiated according to regularity of breathing, presence of body movements, and most important, presence of high-frequency components of breathing (SCSB spikes). With both methods, three sleep/wake stages were distinguished: rapid eye movement (REM) sleep, non-rapid eye movement (NREM) sleep and wakefulness. The average inter-scorer reliability of the PSG sleep staging controlled in nine subjects was 88%. The average concordance between the two methods ranged from 82 to 85%, depending on the criteria used for scoring the SCSB. The mean sensitivity of the SCSB to detect NREM sleep ranged from 77 to 90% and the mean sensitivity to detect REM sleep ranged from 61 to 86%. The mean positive predictive value was 89–96% for NREM sleep and 54–67% for REM sleep. In conclusion, REM sleep is characterized by irregular breathing with superimposed fast respiratory movements. These changes are specific enough to allow distinction between episodes of NREM sleep, REM sleep and wakefulness with the non-invasive SCSB method in infants and young children. Incomplete concordance between PSG and SCSB score was most frequently observed during sleep stage transition periods, where the behavioural state and electrophysiological criteria disagreed. When combined with the PSG, the SCSB provides complementary information about the behavioural state of child.     

Isolated sleep paralysis elicited by sleep interruption.

We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy.     

Estradiol suppresses recovery of REM sleep following sleep deprivation in ovariectomized female rats

Sleep complaints such as insufficient sleep and insomnia are twice as prevalent in women. Symptoms of sleep disruption are often coincident with changes in the gonadal hormone profile across a women's lifespan. Data from a number of different species, including humans, non-human primates and rodents strongly implicate a role for gonadal hormones in the modulation of sleep. In female rats, increased levels of circulating estradiol increase wakefulness and reduce sleep in the dark phase. In this study, we asked whether this reduction in sleep is driven by estradiol-dependent reduction in sleep need during the dark phase by assessing sleep before and after sleep deprivation (SD). Ovariectomized rats implanted with EEG telemetry transmitters were given Silastic capsules containing either 17-β estradiol in sesame oil (E2) or sesame oil alone. After a 24-hour baseline, animals were sleep-deprived via gentle handling for the entire 12-hour light phase, and then allowed to recover. E2 treatment suppressed baseline REM sleep duration in the dark phase, but not NREM or Wake duration, within three days. While SD induced a compensatory increase in REM duration in both groups, this increase was smaller in E2-treated rats compared to oils, as measured in absolute duration as well as by relative increase over baseline. Thus, E2 suppressed REM sleep in the dark phase both before and after SD. E2 also suppressed NREM and increased waking in the early- to mid-dark phase on the day after SD. NREM delta power tracked NREM sleep before and after SD, with small hormone-dependent reductions in delta power in recovery, but not spontaneous sleep. These results demonstrate that E2 powerfully and specifically suppresses spontaneous and recovery REM sleep in the dark phase, and suggest that ovarian steroids may consolidate circadian sleep-wake rhythms.     

Heart rate variability during sleep as a function of the sleep cycle

In this work, in order to evaluate whether autonomic differences distinguish REM sleep and NREM sleep through the whole sleeping period, statistical analysis on spectral power associated with low frequency and high frequency bands were performed on the whole polysomnographic recording, considering the sleep cycle as a unit of sleep. Our results from nine subjects show that power associated with low frequency is higher in REM sleep than in NREM sleep, while power associated with high frequency is significantly higher in NREM sleep than in REM sleep. Differences between REM sleep and NREM sleep are not of the same magnitude within the whole sleep episode and, independent of sleep stages, specific trends are observable in the autonomic control of heart rate during the night.