Slow oscillating transcranial direct current stimulation during sleep has a sleep‐stabilizing effect in chronic insomnia: a pilot study

Recent evidence suggests that lack of slow‐wave activity may play a fundamental role in the pathogenesis of insomnia. Pharmacological approaches and brain stimulation techniques have recently offered solutions for increasing slow‐wave activity during sleep. We used slow (0.75 Hz) oscillatory transcranial direct current stimulation during stage 2 of non‐rapid eye movement sleeping insomnia patients for resonating their brain waves to the frequency of sleep slow‐wave. Six patients diagnosed with either sleep maintenance or non‐restorative sleep insomnia entered the study. After 1 night of adaptation and 1 night of baseline polysomnography, patients randomly received sham or real stimulation on the third and fourth night of the experiment. Our preliminary results show that after termination of stimulations (sham or real), slow oscillatory transcranial direct current stimulation increased the duration of stage 3 of non‐rapid eye movement sleep by 33 ± 26 min (P = 0.026), and decreased stage 1 of non‐rapid eye movement sleep duration by 22 ± 17.7 min (P = 0.028), compared with sham. Slow oscillatory transcranial direct current stimulation decreased stage 1 of non‐rapid eye movement sleep and wake time after sleep‐onset durations, together, by 55.4 ± 51 min (P = 0.045). Slow oscillatory transcranial direct current stimulation also increased sleep efficiency by 9 ± 7% (P = 0.026), and probability of transition from stage 2 to stage 3 of non‐rapid eye movement sleep by 20 ± 17.8% (P = 0.04). Meanwhile, slow oscillatory transcranial direct current stimulation decreased transitions from stage 2 of non‐rapid eye movement sleep to wake by 12 ± 6.7% (P = 0.007). Our preliminary results suggest a sleep‐stabilizing role for the intervention, which may mimic the effect of sleep slow‐wave‐enhancing drugs.     

Sex differences in objective measures of sleep in post‐traumatic stress disorder and healthy control subjects

A growing literature shows prominent sex effects for risk for post‐traumatic stress disorder and associated medical comorbid burden. Previous research indicates that post‐traumatic stress disorder is associated with reduced slow wave sleep, which may have implications for overall health, and abnormalities in rapid eye movement sleep, which have been implicated in specific post‐traumatic stress disorder symptoms, but most research has been conducted in male subjects. We therefore sought to compare objective measures of sleep in male and female post‐traumatic stress disorder subjects with age‐ and sex‐matched control subjects. We used a cross‐sectional, 2 × 2 design (post‐traumatic stress disorder/control × female/male) involving83 medically healthy, non‐medicated adults aged 19–39 years in the inpatient sleep laboratory. Visual electroencephalographic analysis demonstrated that post‐traumatic stress disorder was associated with lower slow wave sleep duration (F_(3,82) = 7.63, P = 0.007) and slow wave sleep percentage (F_(3,82) = 6.11, P = 0.016). There was also a group × sex interaction effect for rapid eye movement sleep duration (F_(3,82) = 4.08, P = 0.047) and rapid eye movement sleep percentage (F_(3,82) = 4.30, P = 0.041), explained by greater rapid eye movement sleep in post‐traumatic stress disorder females compared to control females, a difference not seen in male subjects. Quantitative electroencephalography analysis demonstrated that post‐traumatic stress disorder was associated with lower energy in the delta spectrum (F_(3,82) = 6.79, P = 0.011) in non‐rapid eye movement sleep. Slow wave sleep and delta findings were more pronounced in males. Removal of post‐traumatic stress disorder subjects with comorbid major depressive disorder, who had greater post‐traumatic stress disorder severity, strengthened delta effects but reduced rapid eye movement effects to non‐significance. These findings support previous evidence that post‐traumatic stress disorder is associated with impairment in the homeostatic function of sleep, especially in men with the disorder. These findings suggest that group × sex interaction effects on rapid eye movement may occur with more severe post‐traumatic stress disorder or with post‐traumatic stress disorder comorbid with major depressive disorder.     

Sleep electroencephalographic characteristics of the Cynomolgus monkey measured by telemetry

Cynomolgus monkeys are widely used as models of diseases and in pre‐clinical studies to assess the impact of new pharmacotherapies on brain function and behaviour. However, the time course of electroencephalographic delta activity during sleep, which represents the main marker of sleep intensity associated with recovery during sleep, has never been described in this non‐human primate. In this study, telemetry implants were used to record one spontaneous 24‐h sleep–wake cycle in four freely‐moving Cynomolgus monkeys, and to quantify the time course of electroencephalographic activity during sleep using spectral analysis. Animals presented a diurnal activity pattern interrupted by short naps. During the dark period, most of the time was spent in sleep with non‐rapid eye movement sleep/rapid eye movement sleep alternations and sleep consolidation profiles intermediate between rodents and humans. Deep non‐rapid eye movement sleep showed a typical predominance at the beginning of the night with decreased propensity in the course of the night, which was accompanied by a progressive increase in rapid eye movement sleep duration. Spectral profiles showed characteristic changes between vigilance states as reported in other mammalian species. Importantly, delta activity also followed the expected time course of variation, showing a build‐up with wakefulness duration and dissipation across the night. Thus, Cynomolgus monkeys present typical characteristics of sleep architecture and spectral structure as those observed in other mammalian species including humans, validating the use of telemetry in this non‐human primate model for translational sleep studies.     

EEG sigma and slow‐wave activity during NREM sleep correlate with overnight declarative and procedural memory consolidation

Previous studies suggest that sleep‐specific brain activity patterns such as sleep spindles and electroencephalographic slow‐wave activity contribute to the consolidation of novel memories. The generation of both sleep spindles and slow‐wave activity relies on synchronized oscillations in a thalamo‐cortical network that might be implicated in synaptic strengthening (spindles) and downscaling (slow‐wave activity) during sleep. This study further examined the association between electroencephalographic power during non‐rapid eye movement sleep in the spindle (sigma, 12–16 Hz) and slow‐wave frequency range (0.1–3.5 Hz) and overnight memory consolidation in 20 healthy subjects (10 men, 27.1 ± 4.6 years). We found that both electroencephalographic sigma power and slow‐wave activity were positively correlated with the pre–post‐sleep consolidation of declarative (word list) and procedural (mirror‐tracing) memories. These results, although only correlative in nature, are consistent with the view that processes of synaptic strengthening (sleep spindles) and synaptic downscaling (slow‐wave activity) might act in concert to promote synaptic plasticity and the consolidation of both declarative and procedural memories during sleep.     

NREM sleep EEG slow waves in autistic and typically developing children: Morphological characteristics and scalp distribution

Autism is a developmental disorder with a neurobiological aetiology. Studies of the autistic brain identified atypical developmental trajectories that may lead to an impaired capacity to modulate electroencephalogram activity during sleep. We assessed the topography and characteristics of non‐rapid eye movement sleep electroencephalogram slow waves in 26 boys aged between 6 and 13 years old: 13 with an autism spectrum disorder and 13 typically developing. None of the participants was medicated, intellectually disabled, reported poor sleep, or suffered from medical co‐morbidities. Results are derived from a second consecutive night of polysomnography in a sleep laboratory. Slow waves (0.3–4.0 Hz; >75 µV) were automatically detected on artefact‐free sections of non‐rapid eye movement sleep along the anteroposterior axis in frontal, central, parietal and occipital derivations. Slow wave density (number per minute), amplitude (µV), slope (µV s^?1) and duration (s) were computed for the first four non‐rapid eye movement periods. Slow wave characteristics comparisons between groups, derivations and non‐rapid eye movement periods were assessed with three‐way mixed ANOVAs. Slow wave density, amplitude, slope and duration were higher in anterior compared with most posterior derivations in both groups. Children with autism spectrum disorder showed lower differences in slow waves between recording sites along the anteroposterior axis than typically developing children. These group differences in the topography of slow wave characteristics were stable across the night. We propose that slow waves during non‐rapid eye movement sleep could be an electrophysiological marker of the deviant cortical maturation in autism linked to an atypical functioning of thalamo‐cortical networks.     

Lengthening of the photoperiod influences sleep characteristics before and during total sleep deprivation in rat

The photoperiod has been evidenced to influence sleep regulation in the rat. Nevertheless, lengthening of the photoperiod beyond 30 days seems to have little effect on the 24‐hr baseline level of sleep and the response to total sleep deprivation. We studied the effects of 12:12 (habitual) and 16:8 (long) light–dark photoperiods on sleep, locomotor activity and body core temperature, before and after 24 hr of total sleep deprivation. Eight rats were submitted for 14 days to light–dark 12:12 (lights on: 08:00 hours–20:00 hours) followed by total sleep deprivation, and then for 14 days to light–dark 16:8 (light extended to 24:00 hours) followed by total sleep deprivation. Rats were simultaneously recorded for electroencephalogram, locomotor activity and body core temperature for 24 hr before and after total sleep deprivation. At baseline before total sleep deprivation, total sleep time and non‐rapid eye movement sleep per 24 hr and during extended light hours (20:00 hours–24:00 hours) were higher (13% for total sleep time) after light–dark exposure compared with habitual photoperiod, while percentage delta power in non‐rapid eye movements and rapid eye movements were unchanged. Locomotor activity and body core temperature were lower, particularly during extended light hours (20:00 hours–24:00 hours). Following total sleep deprivation, total sleep time and non‐rapid eye movements were significantly lower after long photoperiod between 20:00 hours and 24:00 hours, and between 10:00 hours and 12:00 hours, and unchanged per 24 hr. The percentage delta power in non‐rapid eye movements was lower between 08:00 hours and 11:00 hours. Total sleep deprivation decreased locomotor activity and body core temperature after habitual photoperiod exposure only. Fourteen days under long photoperiod (light–dark 16:8) increased non‐rapid eye movements sleep, and decreased sleep rebound related to total sleep deprivation (lower non‐rapid eye movements duration and delta power). This may create a model of sleep extension for the rat that has been found to favour anabolism in the brain and the periphery.     

Age affects sleep microstructure more than sleep macrostructure

It is well known that the quantity and quality of physiological sleep changes across age. However, so far the effect of age on sleep microstructure has been mostly addressed in small samples. The current study examines the effect of age on several measures of sleep macro‐ and microstructure in 211 women (22–71 years old) of the ‘Sleep and Health in Women’ study for whom ambulatory polysomnography was registered. Older age was associated with significantly lower fast spindle (effect size f² = 0.32) and K‐complex density (f² = 0.19) during N2 sleep, as well as slow‐wave activity (log) in N3 sleep (f² = 0.21). Moreover, total sleep time (f² = 0.10), N3 sleep (min) (f² = 0.10), rapid eye movement sleep (min) (f² = 0.11) and sigma (log) (f² = 0.05) and slow‐wave activity (log) during non‐rapid eye movement sleep (f² = 0.09) were reduced, and N1 sleep (f² = 0.03) was increased in older age. No significant effects of age were observed on slow spindle density, rapid eye movement density and beta power (log) during non‐rapid eye movement sleep. In conclusion, effect sizes indicate that traditional sleep stage scoring may underestimate age‐related changes in sleep.     

Diurnal changes in electrocorticogram sleep slow‐wave activity during development in rats

According to the homeostatic regulation of sleep, sleep pressure accumulates during wakefulness, further increases during sleep deprivation and dissipates during subsequent sleep. Sleep pressure is electrophysiologically reflected by electroencephalogram slow‐wave activity during non‐rapid eye movement sleep, and is thought to be stable across time. During childhood and adolescence the brain undergoes massive reorganization processes. Slow‐wave activity during these developmental periods has been shown in humans to follow an inverted U‐shaped trajectory, which recently was replicated in rats. The goal of this study was to investigate in rats the diurnal changes of slow‐wave activity during the inverted U‐shaped developmental trajectory of slow‐wave activity. To do so, we performed longitudinal electrocorticogram recordings, and compared the level of slow‐wave activity at the beginning with the slow‐wave activity level at the end of 24‐h baselines in two sets of Sprague–Dawley rats. In younger animals (n = 17) we investigated specific postnatal days when overall slow‐wave activity increases (postnatal day 26), peaks (postnatal day 28) and decreases (>postnatal day 28). The same analysis was performed in older animals (postnatal day 48, n = 6). Our results show a gain of slow‐wave activity across 24 h on postnatal day 26, followed by no net changes on postnatal day 28, which was then followed by a loss of slow‐wave activity during subsequent days (>postnatal day 28). Older animals did not show any net changes in slow‐wave activity across 24 h. These results cannot be explained by differences in vigilance states. Thus, slow‐wave activity during this developmental period may not only reflect the trajectory of sleep pressure but may additionally reflect maturational processes.     

Sleep‐dependent consolidation of face recognition and its relationship to REM sleep duration,REM density and Stage 2 sleep spindles

Face recognition is a highly specialized capability that has implicit and explicit memory components. Studies show that learning tasks with facial components are dependent on rapid eye movement and non‐rapid eye movement sleep features, including rapid eye movement sleep density and fast sleep spindles. This study aimed to investigate the relationship between sleep‐dependent consolidation of memory for faces and partial rapid eye movement sleep deprivation, rapid eye movement density, and fast and slow non‐rapid eye movement sleep spindles. Fourteen healthy participants spent 1 night each in the laboratory. Prior to bed they completed a virtual reality task in which they interacted with computer‐generated characters. Half of the participants (REMD group) underwent a partial rapid eye movement sleep deprivation protocol and half (CTL group) had a normal amount of rapid eye movement sleep. Upon awakening, they completed a face recognition task that contained a mixture of previously encountered faces from the task and new faces. Rapid eye movement density and fast and slow sleep spindles were detected using in‐house software. The REMD group performed worse than the CTL group on the face recognition task; however, rapid eye movement duration and rapid eye movement density were not related to task performance. Fast and slow sleep spindles showed differential relationships to task performance, with fast spindles being positively and slow spindles negatively correlated with face recognition. The results support the notion that rapid eye movement and non‐rapid eye movement sleep characteristics play complementary roles in face memory consolidation. This study also raises the possibility that fast and slow spindles contribute in opposite ways to sleep‐dependent memory consolidation.     

Evidence that non‐dreamers do dream: a REM sleep behaviour disorder model

To determine whether non‐dreamers do not produce dreams or do not recall them, subjects were identified with no dream recall with dreamlike behaviours during rapid eye movement sleep behaviour disorder, which is typically characterised by dream‐enacting behaviours congruent with sleep mentation. All consecutive patients with idiopathic rapid eye movement sleep behaviour disorder or rapid eye movement sleep behaviour disorder associated with Parkinson's disease who underwent a video‐polysomnography were interviewed regarding the presence or absence of dream recall, retrospectively or upon spontaneous arousals. The patients with no dream recall for at least 10 years, and never‐ever recallers were compared with dream recallers with rapid eye movement sleep behaviour disorder regarding their clinical, cognitive and sleep features. Of the 289 patients with rapid eye movement sleep behaviour disorder, eight (2.8%) patients had no dream recall, including four (1.4%) patients who had never ever recalled dreams, and four patients who had no dream recall for 10–56 years. All non‐recallers exhibited, daily or almost nightly, several complex, scenic and dreamlike behaviours and speeches, which were also observed during rapid eye movement sleep on video‐polysomnography (arguing, fighting and speaking). They did not recall a dream following sudden awakenings from rapid eye movement sleep. These eight non‐recallers with rapid eye movement sleep behaviour disorder did not differ in terms of cognition, clinical, treatment or sleep measures from the 17 dreamers with rapid eye movement sleep behaviour disorder matched for age, sex and disease. The scenic dreamlike behaviours reported and observed during rapid eye movement sleep in the rare non‐recallers with rapid eye movement sleep behaviour disorder (even in the never‐ever recallers) provide strong evidence that non‐recallers produce dreams, but do not recall them. Rapid eye movement sleep behaviour disorder provides a new model to evaluate cognitive processing during dreaming and subsequent recall.     

The role of non‐rapid eye movement slow‐wave activity in prefrontal metabolism across young and middle‐aged adults

Electroencephalographic slow‐wave activity (0.5–4 Hz) during non‐rapid eye movement (NREM) sleep is a marker for cortical reorganization, particularly within the prefrontal cortex. Greater slow wave activity during sleep may promote greater waking prefrontal metabolic rate and, in turn, executive function. However, this process may be affected by age. Here we examined whether greater NREM slow wave activity was associated with higher prefrontal metabolism during wakefulness and whether this relationship interacted with age. Fifty‐two participants aged 25–61 years were enrolled into studies that included polysomnography and a ¹⁸[F]‐fluoro‐deoxy‐glucose positron emission tomography scan during wakefulness. Absolute and relative measures of NREM slow wave activity were assessed. Semiquantitative and relative measures of cerebral metabolism were collected to assess whole brain and regional metabolism, focusing on two regions of interest: the dorsolateral prefrontal cortex and the orbitofrontal cortex. Greater relative slow wave activity was associated with greater dorsolateral prefrontal metabolism. Age and slow wave activity interacted significantly in predicting semiquantitative whole brain metabolism and outside regions of interest in the posterior cingulate, middle temporal gyrus and the medial frontal gyrus, such that greater slow‐wave activity was associated with lower metabolism in the younger participants and greater metabolism in the older participants. These results suggest that slow‐wave activity is associated with cerebral metabolism during wakefulness across the adult lifespan within regions important for executive function.     

Interindividual differences in the dynamics of the homeostatic process are trait‐like and distinct for sleep versus wakefulness

The sleep homeostatic Process S reflects the build‐up of sleep pressure during waking and its dissipation during sleep. Process S is modelled as a saturating exponential function during waking and a decreasing exponential function during sleep. Slow wave activity is a physiological marker for non‐rapid eye movement (non‐REM) sleep intensity and serves as an index of Process S. There is considerable interindividual variability in the sleep homeostatic responses to sleep and sleep deprivation. The aim of this study was to investigate whether interindividual differences in Process S are trait‐like. Polysomnographic recordings of 8 nights (12‐h sleep opportunities, 22:00–10:00 hours) interspersed with three 36‐h periods of sustained wakefulness were performed in 11 healthy young adults. Empirical mean slow wave activity per non‐REM sleep episode at episode mid‐points were used for parameter estimation. Parameters of Process S were estimated using different combinations of consecutive sleep recordings, resulting in two to three sets of parameters per subject. Intraclass correlation coefficients were calculated to assess whether the parameters were stable across the study protocol and they showed trait‐like variability among individuals. We found that the group‐average time constants of the build‐up and dissipation of Process S were 19.2 and 2.7 h, respectively. Intraclass correlation coefficients ranged from 0.48 to 0.56, which reflects moderate trait variability. The time constants of the build‐up and dissipation varied independently among subjects, indicating two distinct traits. We conclude that interindividual differences in the parameters of the dynamics of the sleep homeostatic Process S are trait‐like.     

Sleep spindles and rapid eye movement sleep as predictors of next morning cognitive performance in healthy middle‐aged and older participants

Spindles and slow waves are hallmarks of non‐rapid eye movement sleep. Both these oscillations are markers of neuronal plasticity, and play a role in memory and cognition. Normal ageing is associated with spindle and slow wave decline and cognitive changes. The present study aimed to assess whether spindle and slow wave characteristics during a baseline night predict cognitive performance in healthy older adults the next morning. Specifically, we examined performance on tasks measuring selective and sustained visual attention, declarative verbal memory, working memory and verbal fluency. Fifty‐eight healthy middle‐aged and older adults (aged 50–91 years) without sleep disorders underwent baseline polysomnographic sleep recording followed by neuropsychological assessment the next morning. Spindles and slow waves were detected automatically on artefact‐free non‐rapid eye movement sleep electroencephalogram. All‐night stage N2 spindle density (no./min) and mean frequency (Hz) and all‐night non‐rapid eye movement sleep slow wave density (no./min) and mean slope (μV/s) were analysed. Pearson's correlations were performed between spindles, slow waves, polysomnography and cognitive performance. Higher spindle density predicted better performance on verbal learning, visual attention and verbal fluency, whereas spindle frequency and slow wave density or slope predicted fewer cognitive performance variables. In addition, rapid eye movement sleep duration was associated with better verbal learning potential. These results suggest that spindle density is a marker of cognitive functioning in older adults and may reflect neuroanatomic integrity. Rapid eye movement sleep may be a marker of age‐related changes in acetylcholine transmission, which plays a role in new information encoding.     

Shorter duration of non‐rapid eye movement sleep slow waves in EphA4 knockout mice

Slow waves occurring during non‐rapid eye movement sleep have been associated with neurobehavioural performance and memory. In addition, the duration of previous wakefulness and sleep impacts characteristics of these slow waves. However, molecular mechanisms regulating the dynamics of slow‐wave characteristics remain poorly understood. The EphA4 receptor regulates glutamatergic transmission and synaptic plasticity, which have both been linked to sleep slow waves. To investigate if EphA4 regulates slow‐wave characteristics during non‐rapid eye movement sleep, we compared individual parameters of slow waves between EphA4 knockout mice and wild‐type littermates under baseline conditions and after a 6‐h sleep deprivation. We observed that, compared with wild‐type mice, knockout mice display a shorter duration of positive and negative phases of slow waves under baseline conditions and after sleep deprivation. However, the mutation did not change slow‐wave density, amplitude and slope, and did not affect the sleep deprivation‐dependent changes in slow‐wave characteristics, suggesting that EphA4 is not involved in the response to elevated sleep pressure. Our present findings suggest a role for EphA4 in shaping cortical oscillations during sleep that is independent from sleep need.     

Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation

Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non‐rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto‐central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.     

Investigation of sleep spindle activity and morphology as predictors of neurocognitive functioning in medicated patients with schizophrenia

Neurocognitive impairment is a trait marker of schizophrenia, but no effective treatment has yet been identified. Sleep spindle deficits have been associated with diminished sleep‐dependent memory learning. We examined whether this link could be extended into various cognitive domains by investigating the association of a neurocognitive test battery (the Brief Assessment of Cognition in Schizophrenia) with sleep spindle activity and morphology. We examined 37 outpatients diagnosed with schizophrenia and medicated with both antipsychotics and benzodiazepines. Participants underwent 1 night polysomnography and test of neurocognitive functioning. We identified and analysed sleep spindles in all non‐rapid eye movement sleep and in non‐rapid eye movement sleep stage 2 in a central electroencephalography channel using an automatic sleep spindle detector previously validated. Slow sleep spindle density was computed from a frontal electroencephalography channel as well. We found no association between cognitive functioning and sleep spindle density or sleep spindle morphology for spindles in non‐rapid eye movement sleep when controlling for gender, age, symptom severity, and daily dose of antipsychotics and benzodiazepines. For spindles in non‐rapid eye movement sleep stage 2, we found that motor speed was associated with frontal slow sleep spindle density. We conclude that frontal slow spindle density might predict motor speed in medicated patients with schizophrenia, but that no other sleep spindle activity or sleep spindle morphology measures were predictors of neurocognitive functioning.     

Electrodermal activity patterns in sleep stages and their utility for sleep versus wake classification

As the prevalence of sleep disorders is increasing, new methods for ambulatory sleep measurement are required. This paper presents electrodermal activity in different sleep stages and a sleep detection algorithm based on electrodermal activity. We analysed electrodermal activity and polysomnographic data of 43 healthy subjects and 48 patients with sleep disorders. Electrodermal activity was measured using an ambulatory device worn at the wrist. Two parameters to describe electrodermal activity were defined based on previous literature: EDASEF (electrodermal activity‐smoothed feature) as parameter for skin conductance level; and EDAcounts (number of electrodermal activity‐peaks) as skin conductance responses. Analysis of variance indicated significant EDASEF differences between the sleep stages wake versus N1, wake versus N2, wake versus slow‐wave sleep, and wake versus rapid eye movement. The analysis of EDAcounts also showed significant differences, especially in the stages slow‐wave sleep versus rapid eye movement. Between healthy subjects and patients, a significant disparity of EDAcounts was revealed in stage N1. Furthermore, the variances of EDASEF and EDAcounts in N1, N2 slow‐wave sleep and rapid eye movement were higher in the patient group (p [F test] < .05). Next, an electrodermal activity‐based sleep/wake discriminating algorithm was constructed. The optimized algorithm achieved an average sensitivity and specificity for sleep detection of 97% and 75%. The epoch agreement rate (average accuracy) was 86%. These outcomes are comparative to sleep detection algorithms based on actigraphy or heart rate variability. The results of this study indicate that electrodermal activity is not only a robust parameter for describing sleep, but also a potential suitable method for ambulatory sleep monitoring.     

Disrupted rapid eye movement sleep predicts poor declarative memory performance in post‐traumatic stress disorder

Successful memory consolidation during sleep depends on healthy slow‐wave and rapid eye movement sleep, and on successful transition across sleep stages. In post‐traumatic stress disorder, sleep is disrupted and memory is impaired, but relations between these two variables in the psychiatric condition remain unexplored. We examined whether disrupted sleep, and consequent disrupted memory consolidation, is a mechanism underlying declarative memory deficits in post‐traumatic stress disorder. We recruited three matched groups of participants: post‐traumatic stress disorder (n = 16); trauma‐exposed non‐post‐traumatic stress disorder (n = 15); and healthy control (n = 14). They completed memory tasks before and after 8 h of sleep. We measured sleep variables using sleep‐adapted electroencephalography. Post‐traumatic stress disorder‐diagnosed participants experienced significantly less sleep efficiency and rapid eye movement sleep percentage, and experienced more awakenings and wake percentage in the second half of the night than did participants in the other two groups. After sleep, post‐traumatic stress disorder‐diagnosed participants retained significantly less information on a declarative memory task than controls. Rapid eye movement percentage, wake percentage and sleep efficiency correlated with retention of information over the night. Furthermore, lower rapid eye movement percentage predicted poorer retention in post‐traumatic stress disorder‐diagnosed individuals. Our results suggest that declarative memory consolidation is disrupted during sleep in post‐traumatic stress disorder. These data are consistent with theories suggesting that sleep benefits memory consolidation via predictable neurobiological mechanisms, and that rapid eye movement disruption is more than a symptom of post‐traumatic stress disorder.     

Effects of late‐night short‐sleep on in‐home polysomnography: relation to adult age and sex

Bedtime is frequently delayed by many factors in life, and a homeostatic response to the delay may compensate partly for increased time awake and shortened sleep. Because sleep becomes shorter with age and women complain of disturbed sleep more often than men, age and sex differences in the homeostatic response to a delayed bedtime may modify the homeostatic response. The purpose of the present study was to investigate the effect of late‐night short‐sleep (3 h with awakening at about 07:00 hours) on in‐home recorded sleep in men and women in two age groups (20–30 and 65–75 years). Results (N = 59) showed that late‐night short‐sleep was associated with an increase in percentage of N3 sleep and a decrease in percentage of rapid eye movement sleep, as well as decreases in several measures of sleep discontinuity and rapid eye movement density. Men showed a smaller decrease in percentage of rapid eye movement sleep than women in response to late‐night short‐sleep, as did older individuals of both sexes compared with younger. Older men showed a weaker percentage of N3 sleep in response to late‐night short‐sleep than younger men. In general, men showed a greater percentage of rapid eye movement sleep and a lower percentage of N3 sleep than women, and older individuals showed a lower percentage of N3 sleep than younger. In particular, older men showed very low levels of percentage of N3 sleep. We conclude that older males show less of a homeostatic response to late‐night short‐sleep. This may be an indication of impaired capacity for recovery in older men. Future studies should investigate if this pattern can be linked to gender‐associated differences in morbidity and mortality.     

Sleep structure in blindness is influenced by circadian desynchrony

We examined the structure, duration and quality of sleep, including non‐rapid eye movement sleep and rapid eye movement sleep, in 11 blind individuals without conscious light perception and 11 age‐ and sex‐matched sighted controls. Because blindness is associated with a greater incidence of free‐running circadian rhythms, we controlled for circadian phase by a measure of melatonin onset timing. When circadian rhythm was entrained and melatonin onset occurred at normal times, sleep structure did not differ between blind and sighted individuals. On the other hand, an abnormal timing of the circadian phase, including delayed, shifted and unclassifiable melatonin onsets, led to larger rapid eye movement sleep latencies and increased wake times. No differences were observed for stages of non‐rapid eye movement sleep, either between congenital and late blind and sighted individuals, or across the different circadian phases. Moreover, abnormal circadian phases were more common in the blind (n = 5) than the sighted (n = 2) sample. Our findings suggest that the sleep structure of blind individuals depends on entrainment of circadian phase, rather than on the absence of vision.