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.     

Acute exposure to evening blue‐enriched light impacts on human sleep

Light in the short wavelength range (blue light: 446–483 nm) elicits direct effects on human melatonin secretion, alertness and cognitive performance via non‐image‐forming photoreceptors. However, the impact of blue‐enriched polychromatic light on human sleep architecture and sleep electroencephalographic activity remains fairly unknown. In this study we investigated sleep structure and sleep electroencephalographic characteristics of 30 healthy young participants (16 men, 14 women; age range 20–31 years) following 2 h of evening light exposure to polychromatic light at 6500 K, 2500 K and 3000 K. Sleep structure across the first three non‐rapid eye movement non‐rapid eye movement – rapid eye movement sleep cycles did not differ significantly with respect to the light conditions. All‐night non‐rapid eye movement sleep electroencephalographic power density indicated that exposure to light at 6500 K resulted in a tendency for less frontal non‐rapid eye movement electroencephalographic power density, compared to light at 2500 K and 3000 K. The dynamics of non‐rapid eye movement electroencephalographic slow wave activity (2.0–4.0 Hz), a functional index of homeostatic sleep pressure, were such that slow wave activity was reduced significantly during the first sleep cycle after light at 6500 K compared to light at 2500 K and 3000 K, particularly in the frontal derivation. Our data suggest that exposure to blue‐enriched polychromatic light at relatively low room light levels impacts upon homeostatic sleep regulation, as indexed by reduction in frontal slow wave activity during the first non‐rapid eye movement episode.     

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.     

Quality of life in patients with an idiopathic rapid eye movement sleep behaviour disorder in Korea

There have been few quality of life studies in patients with idiopathic rapid eye movement sleep behaviour disorder. We compared the quality of life in idiopathic rapid eye movement sleep behaviour disorder patients to healthy controls, patients with hypertension, type 2 diabetes mellitus without complication and idiopathic restless legs syndrome. Sixty patients with idiopathic rapid eye movement sleep behaviour disorder (24 female; mean age: 61.43 ± 8.99) were enrolled retrospectively. The diagnosis was established based on sleep history, overnight polysomnography, neurological examination and Mini‐Mental State Examination to exclude secondary rapid eye movement sleep behavior disorder. All subjects completed questionnaires, including the Short Form 36‐item Health Survey for quality of life. The total quality of life score in idiopathic rapid eye movement sleep behaviour disorder (70.63 ± 20.83) was lower than in the healthy control group (83.38 ± 7.96) but higher than in the hypertension (60.55 ± 24.82), diabetes mellitus (62.42 ± 19.37) and restless legs syndrome (61.77 ± 19.25) groups. The total score of idiopathic rapid eye movement sleep behaviour disorder patients had a negative correlation with the Pittsburg Sleep Quality Index (r = −0.498, P < 0.001), Insomnia Severity Index (r = −0.645, P < 0.001) and the Beck Depression Inventory‐2 (r = −0.694, P < 0.001). Multiple regression showed a negative correlation between the Short Form 36‐item Health Survey score and the Insomnia Severity Index (β = −1.100, P = 0.001) and Beck Depression Inventory‐2 (β = −1.038, P < 0.001). idiopathic rapid eye movement sleep behaviour disorder had a significant negative impact on quality of life, although this effect was less than that of other chronic disorders. This negative effect might be related to a depressive mood associated with the disease.     

Resistance training does not alter same‐day sleep architecture in institutionalized older adults

Sleep disturbance is a common symptom in institutionalized older adults that reduces their quality of life and may contribute to progression of cognitive impairment. While we found that a 7‐week combination of resistance training, walking and social activity significantly improved sleep in institutionalized older adults compared with a usual care control group, no one to our knowledge has determined the acute effects of resistance training on same‐day sleep in this population. Given the effort required to promote exercise adherence in institutionalized older adults and to obtain a positive training effect, understanding of the acute effects of resistance training on same‐day sleep architecture should be elucidated, especially with respect to unintended consequences. This secondary data analysis assessed if resistance training altered the same‐day sleep architecture in institutionalized older adults. Forty‐three participants (age 81.5 ± 8.1 years, male = 17, female = 26) had two attended overnight polysomnography tests in their rooms for sleep architecture analysis; one polysomnography with same‐day resistance training, one without any resistance training. Resistance training consisted of chest and leg press exercises (three sets, eight repetitions, 80% predicted one‐repetition maximum). There were no significant changes in sleep architecture between either polysomnography nights; sleep efficiency (P = 0.71), time in non‐rapid eye movement stages (P = 0.50), time in rapid eye movement stages (P = 0.14), time awake (P = 0.56), time until sleep onset (P = 0.47), total sleep stage shifts (P = 0.65) or rapid eye movement sleep stage latency (P = 0.57). Our results show no acute same‐day effects of resistance training on sleep architecture in institutionalized older adults. Clinical Trial Registration ClinicalTrials.gov Identifier: NCT00888706.     

Validity,potential clinical utility,and comparison of consumer and research‐grade activity trackers in Insomnia Disorder I: In‐lab validation against polysomnography

Consumer activity trackers claiming to measure sleep/wake patterns are ubiquitous within clinical and consumer settings. However, validation of these devices in sleep disorder populations are lacking. We examined 1 night of sleep in 42 individuals with insomnia (mean = 49.14 ± 17.54 years) using polysomnography, a wrist actigraph (Actiwatch Spectrum Pro: AWS) and a consumer activity tracker (Fitbit Alta HR: FBA). Epoch‐by‐epoch analysis and Bland?Altman methods evaluated each device against polysomnography for sleep/wake detection, total sleep time, sleep efficiency, wake after sleep onset and sleep latency. FBA sleep stage classification of light sleep (N1 + N2), deep sleep (N3) and rapid eye movement was also compared with polysomnography. Compared with polysomnography, both activity trackers displayed high accuracy (81.12% versus 82.80%, AWS and FBA respectively; ns) and sensitivity (sleep detection; 96.66% versus 96.04%, respectively; ns) but low specificity (wake detection; 39.09% versus 44.76%, respectively; p = .037). Both trackers overestimated total sleep time and sleep efficiency, and underestimated sleep latency and wake after sleep onset. FBA demonstrated sleep stage sensitivity and specificity, respectively, of 79.39% and 58.77% (light), 49.04% and 95.54% (deep), 65.97% and 91.53% (rapid eye movement). Both devices were more accurate in detecting sleep than wake, with equivalent sensitivity, but statistically different specificity. FBA provided equivalent estimates as AWS for all traditional actigraphy sleep parameters. FBA also showed high specificity when identifying N3, and rapid eye movement, though sensitivity was modest. Thus, it underestimates these sleep stages and overestimates light sleep, demonstrating more shallow sleep than actually obtained. Whether FBA could serve as a low‐cost substitute for actigraphy in insomnia requires further investigation.     

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.     

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.     

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.     

Arousal responses to respiratory events during sleep: the role of pulse wave amplitude

The study aims at assessing the changes in electroencephalography (as measured by the A‐phases of cyclic alternating pattern) and autonomic activity (based on pulse wave amplitude) at the recovery of airway patency in patients with obstructive sleep apnea syndrome. Analysis of polysomnographic recordings from 20 male individuals with obstructive sleep apnea syndrome was carried out in total sleep time, non‐rapid eye movement and rapid eye movement sleep. Scoring quantified the combined occurrence (time range of 4 s before and 4 s after respiratory recovery) or separate occurrence of A‐phases (cortical activation), and pulse wave amplitude drops (below 30%) to apneas, hypopneas or flow limitation events. A dual response (A‐phase associated with a pulse wave amplitude drop) was the most frequent response (71.8% in total sleep time) for all types of respiratory events, with a progressive reduction from apneas to hypopneas and flow limitation events. The highly significant correlation in total sleep time (r = 0.9351; P < 0.0001) between respiratory events combined with A‐phases and respiratory events combined with pulse wave amplitude drops was confirmed both in non‐rapid eye movement (r = 0.9622; P < 0.0001) and rapid eye movement sleep (r = 0.7162; P < 0.0006). In conclusion, a dual cortical and autonomic activation is the most common manifestation at the recovery of airway patency. The significant correlation between A‐phases and relevant pulse wave amplitude drops suggests a possible role of pulse wave amplitude as a marker of cerebral response to respiratory events.     

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.     

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.     

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.     

REM sleep and muscle atonia in brainstem stroke: A quantitative polysomnographic and lesion analysis study

Important brainstem regions are involved in the regulation of rapid eye movement sleep. We hypothesized that brainstem stroke is associated with dysregulated rapid eye movement sleep and related muscle activity. We compared quantitative/qualitative polysomnography features of rapid eye movement sleep and muscle activity (any, phasic, tonic) between 15 patients with brainstem stroke (N = 46 rapid eye movement periods), 16 patients with lacunar/non-brainstem stroke (N = 40 rapid eye movement periods), 15 healthy controls (N = 62 rapid eye movement periods), and patients with Parkinson's disease and polysomnography-confirmed rapid eye movement sleep behaviour disorder. Further, in the brainstem group, we performed a magnetic resonance imaging-based lesion overlap analysis. The mean ratio of muscle activity to rapid eye movement sleep epoch in the brainstem group (“any” muscle activity 0.09 ± 0.15; phasic muscle activity 0.08 ± 0.14) was significantly lower than in the lacunar group (“any” muscle activity 0.17 ± 0.2, p < 0.05; phasic muscle activity 0.16 ± 0.19, p < 0.05), and also lower than in the control group (“any” muscle activity 0.15 ± 0.17, p < 0.05). Magnetic resonance imaging-based lesion analysis indicated an area of maximum overlap in the medioventral pontine region for patients with reduced phasic muscle activity index. For all groups, mean values of muscle activity were significantly lower than in the patients with Parkinson's disease and polysomnography-confirmed REM sleep behaviour disorder group (“any” activity 0.51 ± 0.26, p < 0.0001 for all groups; phasic muscle activity 0.42 ± 0.21, p < 0.0001 for all groups). For the tonic muscle activity in the mentalis muscle, no significant differences were found between the groups. In the brainstem group, contrary to the lacunar and the control groups, “any” muscle activity index during rapid eye movement sleep was significantly reduced after the third rapid eye movement sleep phase. This study reports on the impact of brainstem stroke on rapid eye movement atonia features in a human cohort. Our findings highlight the important role of the human brainstem, in particular the medioventral pontine regions, in the regulation of phasic muscle activity during rapid eye movement sleep and the ultradian distribution of rapid eye movement-related muscle activity.     

NREM‐related parasomnias in Machado–Joseph disease: clinical and polysomnographic evaluation

Spinocerebellar ataxias (SCA) are autosomal dominant neurodegenerative disorders that affect the cerebellum and its connections, and have a marked clinical and genetic variability. Machado–Joseph disease (MJD) or spinocerebellar ataxia type 3 (SCA3)—MJD/SCA3—is the most common SCA worldwide. MJD/SCA3 is characterized classically by progressive ataxia and variable other motor and non‐motor symptoms. Sleep disorders are common, and include rapid eye movement (REM) sleep behaviour disorder (RBD), restless legs syndrome (RLS), insomnia, excessive daytime sleepiness, excessive fragmentary myoclonus and sleep apnea. This study aims to focus upon determining the presence or not of non‐REM (NREM)‐related parasomnias in MJD/SCA 3, using data from polysomnography (PSG) and clinical evaluation. Forty‐seven patients with clinical and genetic diagnosis of MJD/SCA3 and 47 control subjects were evaluated clinically and by polysomnography. MJD/SCA3 patients had a higher frequency of arousals from slow wave sleep (P < 0.001), parasomnia complaints (confusional arousal/sleep terrors, P = 0.001; RBD, P < 0.001; and nightmares, P < 0.001), REM sleep without atonia (P < 0.001), periodic limb movements of sleep index (PLMSi) (P < 0.001), percentage of N3 sleep (P < 0.001) and percentage of N1 sleep (P < 0.001). These data show that NREM‐related parasomnias must be included in the spectrum of sleep disorders in MJD/SCA3 patients.     

Physiological time structure of the tibialis anterior motor activity during sleep in mice,rats and humans

The validation of rodent models for restless legs syndrome (Willis–Ekbom disease) and periodic limb movements during sleep requires knowledge of physiological limb motor activity during sleep in rodents. This study aimed to determine the physiological time structure of tibialis anterior activity during sleep in mice and rats, and compare it with that of healthy humans. Wild‐type mice (n = 9) and rats (n = 8) were instrumented with electrodes for recording the electroencephalogram and electromyogram of neck muscles and both tibialis anterior muscles. Healthy human subjects (31 ± 1 years, n = 21) underwent overnight polysomnography. An algorithm for automatic scoring of tibialis anterior electromyogram events of mice and rats during non‐rapid eye movement sleep was developed and validated. Visual scoring assisted by this algorithm had inter‐rater sensitivity of 92–95% and false‐positive rates of 13–19% in mice and rats. The distribution of the time intervals between consecutive tibialis anterior electromyogram events during non‐rapid eye movement sleep had a single peak extending up to 10 s in mice, rats and human subjects. The tibialis anterior electromyogram events separated by intervals <10 s mainly occurred in series of two‐three events, their occurrence rate in humans being lower than in mice and similar to that in rats. In conclusion, this study proposes reliable rules for scoring tibialis anterior electromyogram events during non‐rapid eye movement sleep in mice and rats, demonstrating that their physiological time structure is similar to that of healthy young human subjects. These results strengthen the basis for translational rodent models of periodic limb movements during sleep and restless legs syndrome/Willis–Ekbom disease.     

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.     

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.     

Case-control study of subjective and objective differences in sleep patterns in older adults with insomnia symptoms

Older adults have high prevalence rates of insomnia symptoms, yet it is unclear if these insomnia symptoms are associated with objective impairments in sleep. We hypothesized that insomnia complaints in older adults would be associated with objective differences in sleep compared with those without insomnia complaints. To test this hypothesis, we conducted a cross‐sectional study in which older adults with insomnia complaints (cases, n = 100) were compared with older adults without insomnia complaints (controls, n = 100) using dual‐night in‐lab nocturnal polysomnography, study questionnaires and 7 days of at‐home actigraphy and sleep diaries. Cases were noted to have reduced objective total sleep time compared with controls (25.8 ± 8.56 min, P = 0.003). This was largely due to increased wakefulness after sleep onset, and not increased sleep latency. When participants with sleep‐related breathing disorder or periodic limb movement disorder were excluded, the polysomnography total sleep time difference became even larger. Cases also had reduced slow‐wave sleep (5.10 ± 1.38 min versus 10.57 ± 2.29 min, effect size −0.29, P = 0.04). When comparing self‐reported sleep latency and sleep efficiency with objective polysomnographic findings, cases demonstrated low, but statistically significant correlations, while no such correlations were observed in controls. Cases tended to underestimate their sleep efficiency by 1.6% (±18.4%), while controls overestimated their sleep efficiency by 12.4% (±14.5%). In conclusion, we noted that older adults with insomnia complaints have significant differences in several objective sleep findings relative to controls, suggesting that insomnia complaints in older adults are associated with objective impairments in sleep.