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.     

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.     

Human brain activity time-locked to rapid eye movements during REM sleep

To identify the neural substrate of rapid eye movements (REMs) during REM sleep in humans, we conducted simultaneous functional magnetic resonance imaging (fMRI) and polysomnographic recording during REM sleep. Event-related fMRI analysis time-locked to the occurrence of REMs revealed that the pontine tegmentum, ventroposterior thalamus, primary visual cortex, putamen and limbic areas (the anterior cingulate, parahippocampal gyrus and amygdala) were activated in association with REMs. A control experiment during which subjects made self-paced saccades in total darkness showed no activation in the visual cortex. The REM-related activation of the primary visual cortex without visual input from the retina provides neural evidence for the existence of human ponto-geniculo-occipital waves (PGO waves) and a link between REMs and dreaming. Furthermore, the time-course analysis of blood oxygenation level-dependent responses indicated that the activation of the pontine tegmentum, ventroposterior thalamus and primary visual cortex started before the occurrence of REMs. On the other hand, the activation of the putamen and limbic areas accompanied REMs. The activation of the parahippocampal gyrus and amygdala simultaneously with REMs suggests that REMs and/or their generating mechanism are not merely an epiphenomenon of PGO waves, but may be linked to the triggering activation of these areas. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Perception of experimental pain is reduced after provoked waking from rapid eye movement sleep

Patients with chronic pain often complain of pain when they wake at night, but the accuracy of their perception of the pain after waking at night is unknown. While cognitive functions are reduced for a short time after waking from sleep, a situation known as sleep inertia, it is unclear how sleep inertia may affect the perception of pain. We investigated the effects of sleep inertia on the perception of experimentally induced pain. Fourteen male volunteers were exposed to a randomized thermal heat stimulus of 43.1 °C ‘hot’ and 46.5 °C ‘hurting’ during provoked waking from Stage 2 sleep, slow wave sleep and rapid eye movement (REM) sleep. Subjects rated their pain on awakening on a Visual Analogue Scale at 30 s after awakening and each minute thereafter for 5 min. We found no change in pain perception over the 5‐min period irrespective of temperature used or sleep stage. However, perceived pain when awoken abruptly from REM sleep was significantly lower than the awake score for both the hot (P = 0.0069) and hurting (P = 0.0025) temperatures. Pain perception when woken from Stage 2 sleep or slow wave sleep was not significantly different from perception when awake. Our findings indicate that sleep inertia reduces pain perception when awoken abruptly from REM. This suggests that patients who wake up in pain either perceive accurately the pain they are experiencing, or at worst underestimate the level of pain if woken from REM sleep.     

Differential effects of waking from non-rapid eye movement versus rapid eye movement sleep on cardiovascular activity

The occurrence of cardiovascular events increases in the morning, and while the mechanism responsible is yet to be determined, possible contributors include surges in sympathetic activity and concurrent rises in blood pressure (BP). This study tested the hypothesis that the increase in sympathetic dominance and the surge in BP were greater when waking spontaneously from Stage 2 sleep compared with waking from rapid eye movement (REM) sleep. Twenty healthy young adults had overnight polysomnography, including electrocardiogram measurements. Spectral analysis of heart rate variability (HRV) was conducted on 2-min blocks of stable data selected from the last 30 min of sleep and during 30 min of resting wakefulness (supine) immediately following sleep. Outputs included absolute low frequency (LF) and high frequency (HF) power, the LF/HF ratio, heart rate (HR) and BP. To investigate the effect of waking from Stage 2 or REM sleep on HRV and BP responses, two-way analyses of variance ( anova s) (Stage 2 versus REM) with repeated measures (sleep versus morning wakefulness) were performed. It was found that waking from Stage 2 sleep was associated with significant increases in HR ( P  = 0·002) and BP ( P  < 0·001), as well as a tendency towards an increase in the LF/HF ratio ( P  = 0·08), whereas measurements during REM sleep and subsequent wakefulness were similar ( P  > 0·05). The greater increase in BP and HR when waking from Stage 2 sleep compared with REM sleep suggests that in vulnerable populations, waking from Stage 2 sleep could be an adjunct risk factor of cardiovascular events during the morning period.     

GABA in locus coeruleus regulates spontaneous rapid eye movement sleep by acting on GABAA receptors in freely moving rats

The aminergic neurons in the locus coeruleus are known to cease firing during rapid eye movement sleep. Since electrical stimulation of locus coeruleus reduced, while carbachol stimulation increased rapid eye movement sleep and γ-aminobutyric acid (GABA) neurons as well as terminals are present in the locus coeruleus, we hypothesized that GABA may be involved for cessation of locus coeruleus neuronal firing during rapid eye movement sleep. Under surgical anaesthesia male Wistar rats (250–300 g) with bilateral guide cannulae targeting locus coeruleus were prepared for chronic sleep-wakefulness recording. Electroencephalogram (EEG), electrooculogram (EOG), electromyogram (EMG) were recorded in normal, after 250 nl saline and after picrotoxin (250 ng in 250 nl) injection bilaterally into the locus coeruleus. The results showed that mean duration per episode of rapid eye movement sleep was significantly reduced, although its frequency of generation/h was not significantly affected. This study suggests that GABA in locus coeruleus is involved in tonic regulation of rapid eye movement sleep and the action is mediated through GABA_A receptor.     

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.     

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。     

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.     

Local sweating responses during recovery sleep after sleep deprivation in humans

Changes in the central control of sweating were investigated in five sleep-deprived subjects (kept awake for 40 h) during their recovery sleep under warm ambient conditions [operative temperature (T _o) was either 35 or 38° C]. Oesophageal (T _oes) and mean skin (T _sk) temperatures, chest sweat rate (m _sw,ch), and concomitant electro-encephalographic data were recorded. Throughout the night at 35 or 38° C T _o, m _sw,ch changes were measured at a constant local chest skin temperature (T _ch) of 35.5° C. The results showed that body temperatures (T _oes and T _sk) of sleep-deprived subjects were influenced by thermal and hypnogogic conditions. The m _sw,ch levels correlated positively with T _oes in the subjects studied during sleep stage 1–2 (light sleep: LS), sleep stage 3–4 (slow wave sleep: SWS) and rapid eye movement (REM) sleep. Contrary to what has been reported in normal sleep, firstly, the T _oes threshold for sweating onset differed between REM sleep and both LS and SWS, and, secondly, the slopes of the m _sw,ch versus T _oes relationships were unchanged between REM and non-REM (i.e. LS or SWS) sleep. The changes observed after sleep deprivation were hypothesized to be due to alterations in the functioning of the central nervous system controller.     

Fragmentary myoclonus in idiopathic rapid eye movement sleep behaviour disorder

Fragmentary myoclonus is a result of muscle activity consisting of brief potentials in surface electromyography during polysomnography. Excessive fragmentary myoclonus is defined by increased intensity of the potentials. A few studies report excessive fragmentary myoclonus occurrence in neurodegenerative diseases. Because idiopathic rapid eye movement sleep behaviour disorder is considered as an early stage of neurodegeneration with involvement of the brainstem, we charted the prevalence and quantified the intensity of excessive fragmentary myoclonus in idiopathic rapid eye movement sleep behaviour disorder. Twenty‐nine patients (one woman, 28 men, mean age 68 years, SD 6.2) and 29 controls (two women, 27 men, mean age 65.6 years, SD 8.6) underwent polysomnography. Fragmentary myoclonus potentials were identified and counted according to internationally used criteria. Fragmentary myoclonus intensity was quantified by the fragmentary myoclonus index. Excessive fragmentary myoclonus was diagnosed in 75.9% (22 subjects) in idiopathic rapid eye movement sleep behaviour disorder, while in 34.5% (10 subjects) among the controls (p = 0.003). Quantitative analysis showed a wide‐range fragmentary myoclonus index in idiopathic rapid eye movement sleep behaviour disorder (4.0–632.4; median 60.7) and in the controls (0.8–938.1; median 34.3). The overall difference in fragmentary myoclonus index was not significant between the groups; however, patients with idiopathic rapid eye movement sleep behaviour disorder showed trends for higher fragmentary myoclonus index scores in wakefulness (p = 0.027), N1 (p = 0.032), N3 (p = 0.046) and R (p = 0.007). Fragmentary myoclonus index does not correlate with age, idiopathic rapid eye movement sleep behaviour disorder duration or R stage atonia deficiency. The prevalence of excessive fragmentary myoclonus is higher in idiopathic rapid eye movement sleep behaviour disorder compared with the controls, so fragmentary myoclonus should be taken into account in future research of rapid eye movement sleep behaviour disorder and motor control in sleep.     

Non-REM sleep as a source of learning deficits induced by REM sleep deprivation.

Procedures that deprive animal subjects of rapid eye movement sleep have often been associated with learning impairments. Previously, the conclusion has been drawn that these learning impairments are due to the absence of some positive function of rapid eye movement sleep. The present research indicates more precisely that typical impairments associated with the deprivation procedures may be due to isolated periods of non-REM sleep, rather than due to the simple absence of rapid eye movement sleep. Mice were tested for acquistion of a complex maze task, and subjected to post-trial rapid eye movement sleep deprivation by the pedestal method. Only animals demonstrating (non-REM) sleep behaviors during deprivation gave evidence of learning deficits.     

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.     

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.     

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.     

Periodic leg movements during sleep and wakefulness in narcolepsy

The objectives of the study were to measure the prevalence of periodic leg movements during NREM and REM sleep (PLMS) and while awake (PLMW) and to assess the impact of PLMS on nocturnal sleep and daytime functioning in patients with narcolepsy. One hundred and sixty-nine patients with narcolepsy and 116 normal controls matched for age and gender were included. Narcoleptics with high and low PLMS indices were compared to assess the impact of PLMS on sleep and Multiple Sleep Latency Test (MSLT) variables. More narcoleptics than controls had a PLMS index greater than 5 per hour of sleep (67% versus 37%) and an index greater than 10 (53% versus 21%). PLMS indices were higher both in NREM and REM sleep in narcoleptic patients, but the between-group difference was greater for REM sleep. A significant increase of PLMS index was also found with aging in both narcoleptic patients and controls. PLMW indices were also significantly higher in narcoleptic patients. Patients with an elevated index of PLMS had a higher percentage of stage 1 sleep, a lower percentage of REM sleep, a lower REM efficiency and a shorter MSLT latency. The present study demonstrates a high frequency of PLMS and PLMW in narcolepsy, an association between the presence of PLMS and measures of REM sleep and daytime functioning disruption. These results suggest that PLMS represent an intrinsic feature of narcolepsy.     

Tectal activity and eye movements during paradoxical sleep in cats

Phasic negative waves, similar to ponto-geniculo-occipital (PGO) waves, simultaneous with eye movements occurred in the superior colliculus in cats during the desynchronised EEG of paradoxical sleep. The frequency of PGO-like waves in the superior colliculus was about 25% lower than in the lateral geniculate body during the period of eye movements due to absence of 8/sec bursts common in the lateral geniculate body. Eye movements were evoked by stimulating the superior colliculus by rectangular pulse trains, and were accompanied by PGO-like waves in the lateral geniculate body and in the contralateral superior colliculus. During periods of paradoxical sleep, when no spontaneous rapid eye movements and PGO waves occurred, the effect of superior colliculus stimulation decreased. The phasic waves in the superior colliculus are associated apparently with the mechanism of rapid eye movements during paradoxical sleep. They resemble, but are not identical with, the phasic waves recorded under similar conditions in the lateral geniculate body.     

The effect of dream report collection and dream incorporation on memory consolidation during sleep

Collecting dream reports typically requires waking subjects up from their sleep—a method that has been used to study the relationship between dreams and memory consolidation. However, it is unclear whether these awakenings influence sleep‐associated memory consolidation processes. Furthermore, it is unclear how the incorporation of the learning task into dreams is related to memory consolidation. In this study we compared memory performance in a word–picture association learning task after a night with and without awakenings in 22 young and healthy participants. We then examined if the stimuli from the learning task are successfully incorporated into dreams, and if this incorporation is related to the task performance the next morning. We show that while the awakenings impaired both subjective and objective sleep quality, they did not affect sleep‐associated memory consolidation. When dreams were collected during the night by awakenings, memories of the learning task were successfully incorporated into dreams. When dreams were collected in the morning, no incorporations were detected. Task incorporation into non‐rapid eye movement sleep dreams, but not rapid eye movement sleep dreams positively predicted memory performance the next morning. We conclude that the method of awakenings to collect dream reports is suitable and necessary for dream and memory studies. Furthermore, our study suggests that dreams in non‐rapid eye movement rather than rapid eye movement sleep might be related to processes of memory consolidation during sleep.     

Overnight emotional adaptation to negative stimuli is altered by REM sleep deprivation and is correlated with intervening dream emotions

Rapid eye movement (REM) sleep and dreaming may be implicated in cross-night adaptation to emotionally negative events. To evaluate the impact of REM sleep deprivation (REMD) and the presence of dream emotions on a possible emotional adaptation (EA) function, 35 healthy subjects randomly assigned to REMD ( n  = 17; mean age 26.4 ± 4.3 years) and control ( n  = 18; mean age 23.7 ± 4.4 years) groups underwent a partial REMD and control nights in the laboratory, respectively. In the evening preceding and morning following REMD, subjects rated neutral and negative pictures on scales of valence and arousal and EA scores were calculated. Subjects also rated dream emotions using the same scales and a 10-item emotions list. REMD was relatively successful in decreasing REM% on the experimental night, although a mean split procedure was applied to better differentiate subjects high and low in REM%. High and low groups differed – but in a direction contrary to expectations. Subjects high in REMD% showed greater adaptation to negative pictures on arousal ratings than did those low in REMD% ( P  < 0.05), even after statistically controlling sleep efficiency and awakening times. Subjects above the median on EA_valence had less intense overall dream negativity ( P  < 0.005) and dream sadness ( P  < 0.004) than subjects below the median. A correlation between the emotional intensities of the morning dream and the morning picture ratings supports a possible emotional carry-over effect. REM sleep may enhance morning reactivity to negative emotional stimuli. Further, REM sleep and dreaming may be implicated in different dimensions of cross-night adaptation to negative emotions.     

Corticospinal excitability during laughter: implications for cataplexy and the comparison with REM sleep atonia

Cataplexy is usually seen as rapid eye movement (REM) sleep atonia occurring at an inopportune moment. REM sleep atonia is the result of postsynaptic inhibition, i.e. inhibition of alpha motor neurones. Although this may explain the suppression of H-reflexes during REM sleep, cataplexy and laughter, it is not the only explanation. Presynaptic inhibition, in which afferent impulses are prevented from reaching motor neurones, is an alternative. Testing H-reflexes and magnetic-evoked potentials (MEPs) helps to tell them apart: in postsynaptic inhibition MEPs and H-reflexes change in tandem, while H-reflexes may decrease independent of MEPs with other inhibition modes. We studied motor inhibition during laughter, the strongest trigger for cataplexy. H-reflexes were evoked every 2 s in the soleus muscle in 10 healthy subjects watching comical video fragments. MEPs were evoked when H-reflexes decreased during laughter, and, as a control, when subjects did not laugh. Pairs of MEPs and the immediately preceding H-reflexes were studied. Compared with the control condition, laughter caused mean MEP area to increase by 60% (P=0.006) and mean H-reflex amplitude to decrease by 33% (P=0.008). This pattern proves that postsynaptic inhibition cannot have been the sole influence. The findings do not prove which mechanisms are involved; one possibility is that the decrease in H-reflex amplitude was the result of presynaptic inhibition, and that cortical and/or spinal facilitation accounted for increased MEPs. Regardless, the pattern differs fundamentally from the reported mechanism of REM sleep atonia. Existing scanty data on cataplexy suggest a pattern of H-reflexes and MEPs similar to that during laughter, but this needs further study.