Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the rat

An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light-dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle.     

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.     

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.     

Assessing sleepiness in the rat: a multiple sleep latencies test compared to polysomnographic measures of sleepiness

Sleepiness following 6 h of sleep deprivation (SD) was evaluated with a rat multiple sleep latencies test (rMSLT), and the findings were compared to conventional polysomnographic measures of sleepiness. The 6 h of SD was produced by automated activity wheels, and was terminated at either the end of the light period or at the beginning of the dark period. The rMSLT consisted of 5 min wakefulness induced by sensory stimulation followed by 25 min of freedom to sleep. This procedure was repeated every 30 min for 3 h and was designed to minimize the amount of sleep lost due to the testing procedure. In separate rats, 6 h SD was followed by undisturbed recovery, allowing evaluation of conventional polysomnographic measures of sleepiness. Sleep onset latencies were reduced following SD, with recovery in the light (baseline = 8 min, 3 s versus post-SD = 1 min, 17 s) and dark period (baseline = 14 min, 17 s versus 7 min, 7 s). Sleep onset latencies were not altered by varying the duration criterion for the first sleep bout (i.e., sleep bout length criteria of 10, 20, 30, or 60 s were compared). Polysomnographic variables (non-rapid eye movement sleep episode duration, delta power, and number of awakenings) also provided reliable indirect measures of sleepiness, regardless of whether the recovery sleep occurred in the light or dark period. Evaluation of effect size indicated that the rMSLT was a strong measure of sleepiness, and was influenced by homeostatic, circadian, and illumination factors. The rMSLT provided a simple, objective, robust and direct measure of sleepiness that was as effective as conventional polysomnographic measures of sleepiness.     

Identification of a rapid eye movement sleep window for learning of the win‐shift radial arm maze task for male Sprague–Dawley rats

This study identified a rapid eye movement sleep window (RSW) for the eight‐arm win‐shift radial arm maze (RAM) task. The RSW is defined as a period of time after training during which rapid eye movement (REM) sleep is necessary for efficient learning of a task. Rats were trained over a 15‐day period on the win‐shift RAM task. After daily training, groups of rats were deprived of REM sleep using the flowerpot technique or were returned to their cages to serve as controls. Groups were deprived of REM sleep during separate 4‐h intervals, such that the entire 24‐h time‐period after training was investigated for the effects of REM sleep deprivation on learning. The results of the analyses of variance that were calculated for latency to completion data and a measure of the rate of performance improvements, and a survival analysis that was calculated using the first day of maze completion as a censoring variable, indicated that the RSW for the win‐shift task is 0–4 h post‐training.     

Arginine Vasopressin Immunoreactivity is Decreased in the Hypothalamic Suprachiasmatic Nucleus of Subjects with Suprasellar Tumors

Suprasellar tumors with compression of the optic chiasm are associated with an impaired sleep–wake rhythm. We hypothesized that this reflects a disorder of the biological clock of the human brain, the suprachiasmatic nucleus (SCN), which is located just above the optic chiasm. In order to test this hypothesis, we investigated the expression of two key neuropeptides of the SCN, that is, arginine vasopressin (AVP) and vasoactive intestinal peptide (VIP), as assessed by quantitative immunocytochemistry in post‐mortem hypothalamic tissue of patients with a suprasellar tumor inducing permanent visual field defects. Post‐mortem hypothalamic tissue of 5 patients with a suprasellar tumor inducing permanent visual field defects (acromegaly n = 2, nonfunctioning macro‐adenoma n = 1, macroprolactinoma n = 1, infundibular metastasis of a colorectal adenocarcinoma n = 1) and 15 age‐ and gender‐matched controls was obtained from the Netherlands Brain Bank. Total AVP immunoreactivity in the SCN was lower in patients with a suprasellar tumor than in controls (P = 0.03). By contrast, total VIP immunoreactivity was not different between patients and controls (P = 0.44). Suprasellar tumors leading to permanent visual field defects are associated with reduced AVP, but not VIP immunoreactivity, in the SCN. These findings raise the possibility that selective impairment of the SCN contributes to sleep–wake disturbances in these patients.     

Association between proteomics and obstructive sleep apnea phenotypes in a community‐based cohort of women

Proteomic‐based technologies offer new opportunities to identify proteins that might reflect the cardiometabolic stress caused by different aspects of sleep‐disordered breathing. We aimed to investigate whether severe obstructive sleep apnea and severe obstructive sleep apnea during rapid eye movement sleep are associated with changed levels of inflammatory and cardiac disease‐related proteins in a population‐based cohort of women. In the community‐based “Sleep and Health in Women” (SHE) cohort study, 400 women underwent polysomnography, anthropometric measurements and blood sampling. Two proteomic assays (Olink Proseek^® Inflammation panel and Olink Proseek^® Cardiovascular II panel), each measuring 92 proteins, were analysed in a subsample of 253 women. p‐Values were adjusted for multiple testing, with false discovery rate set at 10%. In unadjusted models, 57 proteins were associated with apnea?hypopnea index, 56 proteins with oxygen desaturation index and 64 proteins with rapid eye movement?apnea?hypopnea index. After adjustment for age, body mass index and plate, there were no significant associations between apnea?hypopnea index or oxygen desaturation index and any of the proteins. Severe obstructive sleep apnea during rapid eye movement sleep (rapid eye movement?apnea?hypopnea index ≥ 30) was associated with decreased levels of two anti‐inflammatory proteins; Sirt2 (q‐value .016) and LAP‐TGF‐β₁ (q‐value .016). There was also a negative association between rapid eye movement?apnea?hypopnea index of ≥ 30 and Axin1 (q‐value .095), a protein thought to facilitate TGF‐β‐signalling. We conclude that severe obstructive sleep apnea during rapid eye movement sleep is associated with low levels of Sirt2, LAP‐TGF‐β₁ and Axin1, anti‐inflammatory proteins involved in metabolic regulation and in the atherosclerotic process. For obstructive sleep apnea based on a whole night, the associations with cardiac and inflammatory proteins are weaker, and explained to a large extent by age and body mass index.     

Plasma adiponectin level and sleep structures in children with Prader–Willi syndrome

Adiponectin, an adipose tissue-derived hormone, has been negatively related to obstructive sleep apnea syndrome. Besides sleep apnea, children with Prader–Willi syndrome (PWS) may have excessive daytime sleepiness and rapid eye movement (REM) sleep abnormality. The aim of this study is to determine whether changes in sleep structures are related to plasma adiponectin levels in PWS. Correlations between adiponectin level and sleep variables were analyzed in 28 children with PWS and 18 controls. Overnight polysomnography was performed. The fasting plasma adiponectin levels were higher in the children with PWS than in the controls ( P  =   0.0006). In the PWS, Epworth sleepiness scale was significantly higher ( P  =   0.002); sleep latency ( P  =   0.003) and REM latency ( P  =   0.001) were significantly shortened; the apnea–hypopnea index (AHI) was significantly increased ( P  =   0.0001); and the duration of non-rapid eye movement (NREM) sleep stages 3 and 4 was decreased ( P  =   0.005). Multiple regression analysis revealed correlations between the adiponectin level and the total sleep time ( β  = 0.688, P  =   0.009), AHI ( β  = 1.274, P  =   0.010), REM latency ( β  = −0.637, P  =   0.021) and the percentage of NREM sleep ( β  = −7.648, P  =   0.002) in PWS. In children with PWS, higher plasma adiponectin levels were independently associated with several sleep variables, which was not observed in the control group. These results suggest a potential influence of elevated adiponectin level on the sleep structures in PWS.     

CSF hypocretin-1 (orexin-A) concentrations in narcolepsy with and without cataplexy and idiopathic hypersomnia

We measured cerebrospinal fluid (CSF) hypocretin-1 levels in 11 patients with narcolepsy-cataplexy, five with narcolepsy without cataplexy and 12 with idiopathic hypersomnia (IHS). All patients were Japanese. As reported in Caucasian patients, undetectable or very low hypocretin-1 levels were observed in most (9 out of 11) Japanese narcolepsy--cataplexy patients. Our hypocretin-deficient narcoleptics included three prepubertal cases within few months after the disease onset. All nine hypocretin-deficient patients were human leuckocyte antigen (HLA) DR2 positive, while two who had normal CSF hypocretin-1 levels were HLA DR2 negative. In contrast, none of the narcolepsy without cataplexy and IHS subjects had undetectable low levels. Low CSF hypocretin-1 is therefore very specific for HLA DR2 positive narcolepsy-cataplexy, and the deficiency is likely to be established at the early stage of the disease.     

Quantitative electroencephalography during rapid eye movement (REM) and non‐REM sleep in combat‐exposed veterans with and without post‐traumatic stress disorder

Sleep disturbances are a hallmark feature of post‐traumatic stress disorder (PTSD), and associated with poor clinical outcomes. Few studies have examined sleep quantitative electroencephalography (qEEG), a technique able to detect subtle differences that polysomnography does not capture. We hypothesized that greater high‐frequency qEEG would reflect ‘hyperarousal’ in combat veterans with PTSD (n = 16) compared to veterans without PTSD (n = 13). EEG power in traditional EEG frequency bands was computed for artifact‐free sleep epochs across an entire night. Correlations were performed between qEEG and ratings of PTSD symptoms and combat exposure. The groups did not differ significantly in whole‐night qEEG measures for either rapid eye movement (REM) or non‐REM (NREM) sleep. Non‐significant medium effect sizes suggest less REM beta (opposite to our hypothesis), less REM and NREM sigma and more NREM gamma in combat veterans with PTSD. Positive correlations were found between combat exposure and NREM beta (PTSD group only), and REM and NREM sigma (non‐PTSD group only). Results did not support global hyperarousal in PTSD as indexed by increased beta qEEG activity. The correlation of sigma activity with combat exposure in those without PTSD and the non‐significant trend towards less sigma activity during both REM and NREM sleep in combat veterans with PTSD suggests that differential information processing during sleep may characterize combat‐exposed military veterans with and without PTSD.     

Developmental changes in the sleep electroencephalogram of adolescent boys and girls

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

Hypothalamic Hypocretinergic/Orexinergic Neurons Projecting to the Oral Pontine Rapid Eye Movement Sleep Inducing Site in the Cat

The cat ventral oral pontine reticular nucleus (vRPO) is responsible for the generation and maintenance of rapid eye movement (REM) sleep. Hypothalamic neurons containing the peptide hypocretin‐1 (also called orexin‐A) which will be herewith defined as orexinergic (Orx) neurons, occupy a pre‐eminent place in the integration and stabilization of arousal networks as well as in the physiopathology of narcolepsy/cataplexy. In the previous investigations, low‐volume and dose microinjections of hypocretin‐1 in cat vRPO produced a specific and significant suppression of REM sleep. The aim of this study is to map the hypothalamic Orx neurons that project to the vRPO and suppress REM sleep generation in the cat. Five adult cats received microinjections of the retrograde tracer cholera toxin (CTb) into the vRPO. Brains were processed employing both CTb staining and antiorexin‐A immunocytochemistry techniques. A large number of double‐labeled neurons (Orx–CTb) intermingled with the single CTb‐positive and single Orx neurons were detected in the ipsilateral lateral, perifornical, dorsal, anterior, perimammillothalamic, and posterior hypothalamic areas but were very scarce in the paraventricular, dorsomedial, ventromedial, and periventricular hypothalamic nuclei. A considerable number of double‐labeled neurons were also observed in both the dorsal and the lateral hypothalamic areas in the contralateral hypothalamus. Our results suggest that the widely distributed Orx neuronal hypothalamic groups could physiologically inhibit REM sleep generation in vRPO. Anat Rec, 296:815–821, 2013. © 2013 Wiley Periodicals, Inc.     

Control of hypoglossal motoneurones during naturally occurring sleep and wakefulness in the intact,unanaesthetized cat: a field potential study

The present electrophysiological study was designed to determine the discharge threshold of hypoglossal motoneurones during naturally occurring states of sleep and wakefulness in the intact, unanaesthetized cat. The antidromic field potential, which reflects the net level of membrane excitability of motoneurones and therefore their discharge threshold, was recorded in the hypoglossal nucleus following stimulation of the hypoglossal nerve. The amplitude of the antidromic field potential was larger during wakefulness and non‐rapid eye movement (NREM) sleep compared with REM sleep. There was no significant difference in the amplitude of the field potential when wakefulness was compared with NREM sleep (P = 0.103, df = 3, t = 2.324). However, there was a 46% reduction in amplitude during REM sleep compared with NREM sleep (P < 0.001, df = 10, t = 6.421) or wakefulness (P < 0.01, df = 4, t = ?4.598). These findings indicate that whereas the excitability of motoneurones that comprise the hypoglossal motor pool is relatively constant during wakefulness and NREM sleep, their excitability is significantly reduced during REM sleep. This state‐dependent pattern of control of hypoglossal motoneurones during REM sleep is similar to that reported for motoneurones in other motor nuclei at all levels of the neuraxis. The decrease in the evoked response of hypoglossal motoneurones, which reflects a significant increase in the discharge threshold of individual motoneurones, results in atonia of the lingual and related muscles during REM sleep.     

Temporal association between sleep apnea–hypopnea and sleep bruxism events

There is some evidence suggesting that obstructive sleep apnea–hypopnea syndrome is concomitant with sleep bruxism. The aim of this study was to investigate the temporal association between sleep apnea–hypopnea events and sleep bruxism events. In an open observational study, data were gathered from 10 male subjects with confirmed obstructive sleep apnea–hypopnea syndrome and concomitant sleep bruxism. Polysomnography and audio‐video recordings were performed for 1 night in a sleep laboratory. Breathing, brain, heart and masticatory muscle activity signals were analysed to quantify sleep and sleep stage duration, and number and temporal distribution of apnea–hypopnea events and sleep bruxism events. Apnea–hypopnea events were collected within a 5‐min time window before and after sleep bruxism events, with the sleep bruxism events as the pivotal reference point. Two temporal patterns were analysed: (i) the interval between apnea–hypopnea events termination and sleep bruxism events onset, called T1; and (ii) the interval between sleep bruxism events termination and apnea–hypopnea events onset, called T2. Of the intervals between sleep bruxism events and the nearest apnea–hypopnea event, 80.5% were scored within 5 min. Most intervals were distributed within a period of <30 s, with peak at 0–10 s. The T1 interval had a mean length of 33.4 s and was significantly shorter than the T2 interval (64.0 s; P < 0.05). Significantly more sleep bruxism events were scored in association with the T1 than the T2 pattern (P < 0.05). Thus, in patients with concomitant obstructive sleep apnea–hypopnea syndrome and sleep bruxism, most sleep bruxism events occurred after sleep apnea–hypopnea events, suggesting that sleep bruxism events occurring close to sleep apnea–hypopnea events is a secondary form of sleep bruxism.     

Phasic brain activity related to the onset of rapid eye movements during rapid eye movement sleep: study of event‐related potentials and standardized low‐resolution brain electromagnetic tomography

The function of rapid eye movements (REMs) during REM sleep is still a matter that is open to debate. In a previous study, we found positive brain potential (P200r) time‐locked to the onset of REMs. This potential was not observed during saccades of wakefulness. In this study, we estimated the electrical generation of this potential to investigate the phasic brain activity related to REMs. Data were collected in a sleep laboratory from nine healthy university students. REMs during REM sleep were recorded during natural nocturnal sleep. Event‐related potential time‐locked to the onset of REMs were averaged. Standardized low‐resolution brain electromagnetic tomography (sLORETA) was used to identify the current sources of P200r. The results showed that P200r have neuronal generators in the left premotor area, left primary motor and sensory cortices, left inferior parietal lobule and bilateral occipital areas (precuneus, cuneus and lingual gyrus). All these areas are known to contribute to visuomotor processing. These phasic brain activities might play a key role in explaining the function of REMs during REM sleep.     

快速眼动睡眠剥夺大鼠中缝背核内galanin阳性神经元表达及抑郁行为的研究

目的:研究不同时间快速眼动睡眠剥夺大鼠中缝背核内galanin阳性神经元的表达,抑郁行为的变化以及两者间的相互关系。方法:SD大鼠,雄性,采用完全随机对照分组:正常对照组,24h快速眼动睡眠剥夺组,48h快速眼动睡眠剥夺组,72h快速眼动睡眠剥夺组。用小平台水环境法建立快速眼动睡眠剥夺大鼠模型,正常对照组大鼠常规饲养。分别对各组大鼠进行强迫游泳实验,悬尾实验,记录抑郁行为得分;然后对各组大鼠脑片进行免疫荧光组化染色,检测中缝背核内galanin阳性神经元的表达。结果:各快速眼动睡眠剥夺组大鼠抑郁行为的得分较正常对照组均增高,尤以72h快速眼动睡眠剥夺组的得分较高,同时,各快速眼动睡眠剥夺组大鼠中缝背核内galanin阳性神经元的数量较正常对照组均增多,尤其以72h快速眼动睡眠剥夺组阳性神经元的表达增多显著。结论:galanin参与快速眼动睡眠剥夺发生后的生物学效应,中缝背核内galanin阳性神经元的表达上调可能与快速眼动睡眠剥夺大鼠抑郁行为的变化有关。     

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.     

Eye movements in idiopathic rapid eye movement sleep behaviour disorder: High antisaccade error rate reflects prefrontal cortex dysfunction

Abnormalities of eye movements have been reported in patients with Parkinson's disease (PD). However, it is unclear if they occur in the prodromal stage of synucleinopathy represented by idiopathic rapid eye movement sleep behaviour disorder (iRBD). We thus aimed to study eye movements in subjects with iRBD and in de novo PD, to assess if their abnormalities may serve as a clinical biomarker of neurodegeneration. Fifty subjects with polysomnography‐confirmed iRBD (46 male, age 40–79 years), 18 newly diagnosed, untreated PD patients (13 male, age 43–75 years) and 25 healthy controls (20 male, age 42–79 years) were prospectively enrolled. Horizontal and vertical ocular prosaccades and antisaccades were investigated with video‐oculography. All patients completed the MDS‐UPDRS and the Montreal Cognitive Assessment. In addition, a neuropsychological battery was performed on iRBD subjects. When compared with healthy controls, both de novo PD patients and iRBD subjects showed increased error rates in the horizontal antisaccade task (p < 0.01, p < 0.05 respectively). In the iRBD group, the error rates in horizontal and vertical antisaccades correlated with performances in the Prague Stroop Test and the Grooved Pegboard Test, as well as with motor scores of the MDS‐UPDRS. De novo PD patients showed a lower gain (p < 0.01) compared with controls. In conclusion, the increased error rate in the antisaccade task of iRBD and PD patients reflects a dysfunction of the dorsolateral prefrontal cortex and is related to the impairment of executive functions and attention.     

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.     

Cold exposure impairs dark-pulse capacity to induce REM sleep in the albino rat

In the albino rat, a REM sleep (REMS) onset can be induced with a high probability and a short latency when the light is suddenly turned off (dark pulse, DP) during non-REM sleep (NREMS). The aim of this study was to investigate to what extent DP delivery could overcome the integrative thermoregulatory mechanisms that depress REMS occurrence during exposure to low ambient temperature (Ta). To this aim, the efficiency of a non-rhythmical repetitive DP (3 min each) delivery during the first 6-h light period of a 12 h:12 h light-dark cycle in inducing REMS was studied in the rat, through the analysis of electroencephalogram, electrocardiogram, hypothalamic temperature and motor activity at different Tas. The results showed that DP delivery triggers a transition from NREMS to REMS comparable to that which occurs spontaneously. However, the efficiency of DP delivery in inducing REMS was reduced during cold exposure to an extent comparable with that observed in spontaneous REMS occurrence. Such impairment was associated with low Delta activity and high sympathetic tone when DPs were delivered. Repetitive DP administration increased REMS amount during the delivery period and a subsequent negative REMS rebound was observed. In conclusion, DP delivery did not overcome the integrative thermoregulatory mechanisms that depress REMS in the cold. These results underline the crucial physiological meaning of the mutual exclusion of thermoregulatory activation and REMS occurrence, and support the hypothesis that the suspension of the central control of body temperature is a prerequisite for REMS occurrence.