The influence of pre-sleep cognitive arousal on sleep onset processes

Cognitive hyperarousal, resulting in enhanced cognitive activation, has been cited as an important contributor to the development and preservation of insomnia. To further understand this process, our study examined the effects of acutely-induced pre-sleep cognitive hyperarousal on sleep onset processes in healthy volunteers. Following an adaptation night, 15 subjects slept two nights in our sleep laboratory: one reference night and another one with cognitive arousal induction, in a counterbalanced order. In the cognitive arousal condition, subjects worked through half an hour of cognitive tasks without interference of an emotional component prior to retiring to bed. Objective sleep onset latency was significantly prolonged in the cognitive arousal condition compared to the reference condition. Significantly more high frequency activity was recorded during the first and second deep-sleep period. Moreover, differences in heart rate and proximal temperature during and after sleep onset were observed in the nights after the cognitive induction. Pre-sleep cognitive activation successfully induced a significant cognitive load and activation in our subjects to influence subsequent sleep (onset) processes.     

Variability and predictability in sleep patterns of chronic insomniacs

Sleep of chronic insomniacs is often characterized by extensive night-to-night variability. To date, no study has examined this variability with long series of daily sleep data. The present study examined night-to-night variability with a sample of 106 participants meeting DSM-IV diagnostic criteria for persistent primary insomnia. Participants completed daily sleep diaries for an average of 31 days (range: 18-56). Sleep efficiency, sleep onset latency and wake after sleep onset were derived from this measure. Despite evidence of extensive night variability, results showed that sleep patterns could be classified in three clusters. The first one was characterized by a high probability of having poor sleep, the second one by a low and decreasing probability, and the third one by a constant median probability of having a poor sleep, which is an unpredictable sleep pattern. In the first cluster, poor sleep was expected each night for patients with a predominance mixed insomnia including the three insomnia subtypes. In the second cluster, patients presented moderate insomnia, sleep-onset latency below the threshold level and a predominance of sleep-maintenance insomnia. In the third pattern, poor nights seemed unpredictable for patients with moderate to severe insomnia associated with the lowest proportion of sleep-maintenance insomnia. Overall, sleep was predictable for about two-thirds of individuals, whereas it was unpredictable for about one-third. These findings confirm the presence of extensive variability in the sleep of chronic insomniacs and that poor sleep may be predictable for some of them. Additional research is needed to characterize those sleep patterns in terms of clinical features and temporal course.     

Presleep cognitions and attributions in sleep-onset insomnia

This research examined the role of cognitive factors (attributions about the causes of sleep difficulties and presleep cognitive activity) in sleep-onset insomnia. Thirty-four subjects, including 13 mild to extreme insomniacs, were interviewed and then spent 5 consecutive nights in a sleep laboratory. In a multiple regression paradigm predictor measures included attribution ratings of sleep difficulty, perceived control of presleep cognitions, presleep cognitive content, and affect associated with presleep cognitions. Criterion measures included laboratory measured objectives and subjective sleep-onset latency, a score presenting the difference between objective and subjective laboratory measures of sleep-onset latency, interview-measured subjective sleep-onset latency, and degree of overall concern and presleep concern about initiating sleep. The results of multiple regression analyses suggested that the content of presleep cognitions and the attributions of sleep difficulties were significantly associated with several subjective measures of sleep-onset latency or concern with initiating sleep. None of the predictor measures was significantly associated with objectively measured sleep-onset latency. Implications for cognitive theories of sleep-onset insomnia and for the psychophysiologic-subjective dimension of insomnia are discussed.The authors would like to express their appreciation for the assistance provided by Wade Horn, Linda Gannon, Paula Heiser, Sarah Dickson, Kathy Kyndberg, A. E. Adams, IV, and Bill Hoffman.     

Effects of sleep deprivation on spontaneous arousals in humans

STUDY OBJECTIVES: The hierarchical definition of arousals from sleep includes a range of physiologic responses including microarousals, delta and K-complex bursts, and variations in autonomic system. Whether patterns in slow-wave electroencephalographic activity and autonomic activation are primary forms of arousal response can be addressed by studying effects of total sleep deprivation. We therefore examined changes in arousal density during recovery sleep in healthy subjects. DESIGN: Participants spent 6 consecutive 24-hour periods in the laboratory. Nights 1 and 2 were baseline nights followed by 64-hour total sleep deprivation, then 2 consecutive recovery nights. SETTING: Sleep-deprivation protocol was conducted under laboratory conditions with continuous behavioral and electrophysiologic monitoring. PARTICIPANTS: Twelve drug-free men aged 27.4 +/- 7.9 years were studied. None reported sleepiness or altered sleep-wake cycle, and none had neurologic, psychiatric or sleep disorders. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Arousals were classified into 4 levels: microarousals, phases of transitory activation, and delta and K-complex bursts. Sleep deprivation induced changes in the density of considered arousals except phases of transitory activation, with a distinct pattern among the different types. The greatest change was found for microarousals, which showed a significant decrease in the first recovery night (P = .01), with return to baseline thereafter. A fall in K-complex and delta-burst density was noted in the first recovery night, not, however, reaching statistical significance. The phases of transitory activation rate were virtually unaffected throughout the experimental nights. CONCLUSIONS: We conclude that homeostatic sleep processes exert an inhibitory effect on arousal response from sleep with a significant effect only on the microarousal density. Decreased delta and K-complex burst rates, though not significant, support the hypothesis that they may be activating processes, probably modulated by factors independent from those implicated in cortical arousal.     

Arousals and sleep stages in patients with obstructive sleep apnoea syndrome: changes under nCPAP treatment

Nocturnal arousals are the essential cause of disturbed sleep structure in patients with obstructive sleep apnoea syndrome (OSAS). The aim of this study was to analyse the relationship between sleep stages, respiratory (type-R) and movement (type-M) related EEG arousals. Furthermore, the value of these arousals as a criterion for the efficiency of nCPAP treatment was estimated. We examined 38 male patients aged between 30 and 71 (49.1±20.9 SD) y. All patients suffered from OSAS. The mean respiratory disturbance index (RDI) was 47.3±27.8 per h. Polysomnographic monitoring was carried out on 4 subsequent nights: baseline night, 2 nights of nCPAP titration and nCPAP control night. Sleep was visually scored and EEG arousals were classified into type R and M, depending on whether changes of respiration or movement caused the arousal. The RDI, the R index (type-R/h), the M index (type-M/h) and the R and M indices in different sleep stages were calculated. During the baseline night a deficit of slow wave sleep (SWS) and REM sleep was found. Furthermore there were more type-R than type-M arousals registered (17.4 h^?1[3.6–43.6] vs. 5.9 h^?1[1.6–11.8]) ( P <0.01). They occurred during stages NREM 1, NREM 2 and REM ( P <0.01). An SWS sleep rebound and a reduction of the SWS and REM latencies were already found during the first CPAP night. The R index was reduced during the first CPAP night in all sleep stages ( P <0.01) and remained approximately the same in the following 2 nights (3. CPAP night: 1.1 h^?1[0.3–5.0]). Type M arousals occurred more in stages 1 and 2 ( P <0.01), and remained unchanged under nCPAP. We concluded that differentiation of nocturnal arousals may provide more detailed information regarding the influence of breathing disturbances on sleep. Respiratory related, not movement related, arousals may be a useful additional tool in judging the efficiency of OSAS.     

Retrograde effects of triazolam and zolpidem on sleep-dependent motor learning in humans

Drugs that act as allosteric activators at the benzodiazepine site of the gamma-aminobutyric acid (GABA_A) receptor complex are used commonly to treat insomnia but relatively little is known of how such use affects learning and memory. Although anterograde effects on memory acquisition have been shown, possible retrograde effects on consolidation are more relevant when such agents are administered at bedtime. We tested the effects of two GABA_A allosteric activators on sleep-dependent motor skill memory consolidation in 12 healthy male subjects. Subjects slept in a sleep laboratory for four consecutive nights (one accommodation night followed by three experimental nights). Placebo, triazolam 0.375 mg, and zolpidem 10 mg were given to each subject in counterbalanced order on the experimental nights. Polysomnographic (PSG) sleep measurement and sleep-dependent motor learning were assessed at each condition. Triazolam was associated with longer total sleep time and increased Stage 2 sleep. Both zolpidem and triazolam were associated with increased latency to rapid eye movement (REM) sleep. Overnight motor learning correlated with total sleep time in the placebo condition but not in the triazolam or zolpidem conditions. A statistically significant impairment in motor performance occurred overnight in the triazolam condition only. Triazolam, given in sufficient doses to prolong sleep in healthy people, affected overnight motor learning adversely. Zolpidem, in a dose sufficient to prolong REM onset latency but without other effects on PSG-measured sleep, degraded the relationship between total sleep time and overnight motor learning. These data indicate that non-selective or α1-preferring benzodiazepine site allosteric activators can interfere with sleep-dependent memory consolidation.     

Training subjective insomniacs to accurately perceive sleep onset.

Subjective insomniacs overestimate sleep latency at the beginning of their nocturnal sleep period. It was hypothesized that subjective insomniacs could be trained to accurately estimate sleep latency by learning to differentiate wakefulness from sleep. Ten subjective insomniacs were randomly assigned to one of two groups. Group 1 subjects participated in both a control and a training week; group 2 subjects participated only during a training week. Each week consisted of a baseline lab night, a training lab night (treatment or control), a home (unmonitored night) and a recovery lab night. During training, subjects were taught to use sleep markers (A, B or C) to help them more accurately estimate sleep latency and were given feedback about the accuracy of their estimates. Marker A corresponded to an electroencephalographic level of wakefulness; marker B corresponded to the initial sleep spindle; marker C corresponded to 5 minutes of continuous sleep after the first sleep spindle. In the control condition, subjects had no feedback and were not taught to use markers to help them judge sleep from wakefulness. Total sleep time and percent stage 3 sleep increased, and objective sleep latency decreased on recovery nights. After training, subjective sleep latency, correctness of estimates of sleep versus wakefulness and perceived ability to fall asleep significantly improved. This study helps to establish that subjective insomniacs can learn to more accurately estimate sleep from wakefulness with the use of sleep-wake markers.     

Frontalis Muscle Tension and Sleep Latency

This study examined the relationship between frontalis muscle tension and sleep latency. Fifteen subjects reporting various sleep latencies participated. In addition to recording frontalis muscle tension, sleep was monitored on a polygraph for 3 nights. Contrary to expectation, the waking frontalis EMG level did not predict sleep latency. If future research were to show a similar lack of relationship between tension in other muscle groups and sleep onset, it would call into question the use of muscle relaxant drugs and muscle relaxation training in the treatment of sleep-onset insomnia.     

Slow-wave sleep deprivation and waking function

SUMMARY  Slow-wave sleep (SWS) has been theorized to be an intense form of nonREM sleep, but selective deprivation of SWS or Stage 4 sleep has not been shown to cause greater decrements in alertness or performance, compared to deprivation or disruption of the other stages of sleep. The present experiment examined the effects of marked SWS deprivation (SD) for two nights, a control sleep disruption (CD) condition in which minutes of SWS were preserved, and a no sleep disruption (ND) condition. Daytime sleepiness was assessed with the multiple sleep latency test (MSLT) and performance was evaluated with the simulated assembly line task (SALT), neither of which was used in previous studies of SWS or Stage 4 sleep deprivation. In agreement with prior studies, two nights of SD did not cause greater daytime sleepiness than did CD, although sleepiness in both conditions was increased compared to the ND condition. In addition, neither SD nor CD caused declines in performance or mood. However, post hoc analysis suggests an interaction between SWS and sleep duration, such that sufficient SWS may tend to prevent adverse effects of mild sleep loss on waking function.     

Alpha‐wave frequency characteristics in health and insomnia during sleep

Appearances of alpha waves in the sleep electrencephalogram indicate physiological, brief states of awakening that lie in between wakefulness and sleep. These microstates may also cause the loss in sleep quality experienced by individuals suffering from insomnia. To distinguish such pathological awakenings from physiological ones, differences in alpha‐wave characteristics between transient awakening and wakefulness observed before the onset of sleep were studied. In polysomnographic datasets of sleep‐healthy participants (n = 18) and patients with insomnia (n = 10), alpha waves were extracted from the relaxed, wake state before sleep onset, wake after sleep‐onset periods and arousals of sleep. In these, alpha frequency and variability were determined as the median and standard deviation of inverse peak‐to‐peak intervals. Before sleep onset, patients with insomnia showed a decreased alpha variability compared with healthy participants (P < 0.05). After sleep onset, both groups showed patterns of decreased alpha frequency that was lower for wake after sleep‐onset periods of shorter duration. For patients with insomnia, alpha variability increased for short wake after sleep‐onset periods. Major differences between the two groups were encountered during arousal. In particular, the alpha frequency in patients with insomnia rebounded to wake levels, while the frequency in healthy participants remained at the reduced level of short wake after sleep‐onset periods. Reductions in alpha frequency during wake after sleep‐onset periods may be related to the microstate between sleep and wakefulness that was described for such brief awakenings. Reduced alpha variability before sleep may indicate a dysfunction of the alpha generation mechanism in insomnia. Alpha characteristics may also prove valuable in the study of other sleep and attention disorders.     

A complementary relationship between wake and REM sleep in the auditory system: a pre-sleep increase of middle-ear muscle activity (MEMA) causes a decrease of MEMA during sleep

Since some evidence has supported a complementary relationship between waking and REM-sleep eye movement (variations in frequency, amplitude, or direction of waking saccades have been found to inversely affect the corresponding parameters of rapid eye movements), the present study assessed whether this relationship can also be shown for other phasic components of REM sleep, such as middle-ear muscle activity (MEMA), as a consequence of an increase of middle-ear reflex frequency during pre-sleep wake. Ten subjects were studied in three consecutive nights (one adaptation, one baseline, one experimental). In the experimental night, subjects underwent a 2-h pure-tone (1000 Hz, 90 dB SPL) auditory stimulation and MEMA was monitored every 15 min; noise exposure during daytime was also controlled. Results show that MEMA frequency during REM sleep significantly decreased during the experimental nights compared with baseline nights, while each sleep variable as well as mean daily auditory input did not present any significant difference between baseline and experimental nights. Results suggest that the complementary relationship between wake and REM sleep is not bounded to oculomotor activity, but it may also be extended at least to middle-ear muscle phasic activity. Received: 30 April 1999 / Accepted: 14 September 1999     

The effect of clustered versus regular sleep fragmentation on daytime function

Previously, we found that regular sleep fragmentation, similar to that found in patients with sleep apnoea/hypopnoea syndrome (SAHS), impairs daytime function. Apnoeas and hypopnoeas occur in groups in patients with REM or posture related SAHS. Thus, we hypothesised that clustered sleep fragmentation would have a similar impact on daytime function as regular sleep fragmentation. We studied 16 subjects over two pairs of 2 nights and 2 days. The first night of each pair was for acclimatisation. On the second night, subjects either had their sleep fragmented regularly every 90 s, or fragmented every 30 s for 30 min every 90 min, the remaining 60 min being undisturbed. We fragmented sleep with tones to produce a minimum 3 s increase in EEG frequency. During the days following each pair of nights we tested subjects daytime function. Total sleep time (TST) and microarousal frequency were similar no both study nights. We found significantly less stage 2 (55 SD 4, 62 +/- 7%; P = 0.001) and more slow wave sleep (21 SD 3, 12 +/- 6%; P < 0.001) on the clustered night. Mean sleep onset latency was similar on MSLT (clustered 10 SD 5, regular 9 +/- 4 min; P = 0.7) and MWT (clustered 32 SD 7, regular 30 +/- 7 min; P = 0.2). There was no difference in subjects mood or cognitive function after either study night. These results suggest that although there is more slow wave sleep (SWS) on the clustered night, similar numbers of sleep fragmenting events produced similar daytime function whether the events were evenly spaced or clustered.     

Microarousals in patients with sleep apnoea/hypopnoea syndrome

SUMMARY Upper airway obstructions during sleep cause recurrent brief awakenings or microarousals. Standard criteria exist for sleep and respiratory event scoring, however, there are different definitions currently used to score microarousals. We therefore compared three definitions of microarousal (ranging from 1.5-3 s in duration) and one of awakening (> 15 s). We examined their occurrence at the termination of apnoeas and hypopnoeas and their correlation with daytime sleepiness in patients with sleep apnoea/hypopnoea syndrome (SAHS). Sixty-three patients (aged 49, SD 10) had overnight polysomnography, multiple sleep latency tests (MSLT) and Epworth Sleepiness Scales (ESS). There were significantly more microarousals by any definition than there were awakenings (P<0.001) and there were more 1.5 s than 3 s microarousals (P<0.001). Significantly more apnoeas and hypopnoeas were terminated by 1.5 s microarousals (83% and 81%) than by 3 s microarousals (75%) (all P<0.001). Apnoea/hypopnoea index (AHI) correlated significantly with objective daytime sleepiness (p = -0.30, P<0.01). There were weakly significant relationships between all three microarousal definitions (-0.24<P< -0.22, 0.03<P<0.04) and objective daytime sleepiness. None of the arousal definitions correlated with Epworth Sleepiness Scales scores. These results suggest that although 1.5 s microarousals are found at the end of more respiratory events, relationships between 3 and 1.5 s definitions, and daytime sleepiness are similar. This indicates that any of the three microarousal definitions can be used for visual assessment of sleep fragmentation.     

The impact of five nights of sleep restriction on emotional reactivity

An inadequate amount of sleep can negatively affect emotional processing, causing behavioural and neurofunctional changes. However, unlike the condition of total sleep deprivation, which has been extensively studied, the effects of prolonged sleep restriction have received less attention. In this study, we evaluated, for the first time, the effects of five nights of sleep restriction (5 hr a night) on emotional reactivity in healthy subjects. Forty‐two subjects were selected to participate, over two consecutive weeks, in two experimental conditions in counterbalanced order. The subjects were tested the morning after five nights of regular sleep and after five consecutive nights of sleep restriction. During the test, participants evaluated valence and arousal of 90 images selected from the International Affective Picture System. The subjects perceived pleasant and neutral pictures in a more negative way in the sleep‐restriction condition compared to the sleep condition. This effect survived after removing the contribution of mood changes. In contrast, there was no significant difference between conditions for ratings of unpleasant pictures. These results provide the first evidence that an inadequate amount of sleep for five consecutive nights determines an alteration of the evaluation of pleasant and neutral stimuli, imposing a negative emotional bias. Considering the pervasiveness of insufficient sleep in modern society, our results have potential implications for daily life, as well as in clinical settings.     

Performance and sleepiness following moderate sleep disruption and slow wave sleep deprivation

Recent studies have shown that periodically disrupted sleep resulted in significant daytime sleepiness and performance loss in normal young adults. One study suggested that the periodicity of disturbance rather than the total number of sleep disturbances was the primary factor in causing degraded function. However, in that study, increased performance levels could have been associated with increased levels of slow wave sleep. The present study was designed to determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep. Twelve normal young adults spent two 4-night periods in the laboratory. During one 4-night series, Ss were briefly aroused either following each 10 min of sleep or whenever they entered stage 3 sleep (No SWS condition). During the second series of nights, Ss were briefly aroused after each 10 min of sleep (SWS condition). In the second series, additional arousals were performed after 5-min periods (but not when Ss were in SWS) to equalize the total number of arousals in the SWS conditions with those in the No SWS condition. Total experimental arousals were equal in the disruption conditions, and the experimental manipulation was successful in reducing total SWS to infrequent epochs of stage 3 in the No SWS condition while allowing significantly more SWS in the SWS condition. In terms of sleep stages, this difference was balanced by increased stage 2 in the No SWS condition. Despite the differential occurrence of SWS, no performance, mood, or nap latency measure was different in the SWS vs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of sleep condition and sleep-related psychological activity after cognitive-behavior and pharmacological therapy for chronic insomnia

BACKGROUND: Previous studies of insomnia focused mainly on the improvement of sleep condition and ignored the effects of sleep-related psychological activity and daytime function after pharmacological and behavioral treatments. We compared the clinical effects of both therapies on sleep condition, sleep-related psychological activity and daytime function in chronic insomnia. METHODS: Seventy-one patients with chronic insomnia were randomly divided into 4 groups and either received cognitive-behavior therapy (CBT, n = 19), pharmacological therapy (PCT, n = 17), CBT plus medication (Combined, n = 18) or placebo (n = 17). The treatments lasted for 8 weeks with follow-ups conducted at 3 and 8 months. On the day after treatment ended, all patients were assessed using a polysomnogram (PSG), a sleep diary and a psychological assessment. RESULTS: The three active treatments were more effective than placebo at the time the treatments were completed. Subjective sleep-onset latency, sleep efficacy and total sleep time were better in the PCT group than in the CBT group. At the 3-month follow-up, subjective and objective sleep-onset latency, sleep efficacy and total sleep time were better in the CBT group than in both the PCT and the Combined group. At the 8-month follow-up, the CBT group showed a steady comfortable sleep state, while the PCT and Combined groups were gradually returning to the pre-treatment condition. The Combined group showed a variable long-term effect. On the other hand, pre-sleep arousal at nighttime, dysfunctional beliefs about sleep as well as daytime functioning in the CBT group not only improved, but was better than in the other active treatment groups. CONCLUSION: Medication and Combined therapy produced a short-term effect on chronic insomnia while CBT had a long-term effect of improved sleep-related psychological activity and daytime functioning.     

Chemosensory induced arousals during sleep in premenopausal women

Only a limited number of studies is available addressing chemosensory stimulation during sleep. Recent work indicates that stimulation with a nasal irritant produces an increase in arousal frequency in non-REM sleep, whereas a selective olfactory stimulant does not. The present study focused on arousal reactions in REM sleep. Five young healthy volunteers were investigated during 27 nights. Using air-dilution olfactometry CO(2) was used for nasal irritation and H(2)S was used as a specific olfactory stimulant. Both stimuli were presented at four concentrations, odorless stimuli served as control. Other than in previous studies arousal latency was used as a dependent measure. Even the strongest olfactory stimulus did not produce an increase in arousal frequency in REM sleep whereas for irritation such an increase was clearly present. Latencies of arousal responses to CO(2) shortened with increasing stimulus concentrations. Olfactory stimulation does not lead to arousal reactions. In contrast, trigeminal stimulation produces a concentration-dependent increase in arousal frequency and decrease in arousal latency across all sleep stages. The present data shows for the first time that arousals are not present during REM sleep in response to selective olfactory stimuli. However, such changes are easily evoked by irritants activating the trigeminal nerve.     

Behavioral Control of Respiration in Sleep and Sleepiness Due to Signal-Induced Sleep Fragmentation

The effects of sleep fragmentation on behavioral control of sleeping respiration and on daytime sleepiness were investigated in 20 college students. All were polygraphically monitored both during nighttime sleep and during daytime naps. Ten experimental subjects were informed while awake that tones would be presented to them during nighttime sleep. Their task was to terminate the tones by taking a deep breath. Half of the subjects first received tones every 4 min; the other half received them every 8 min. After 4 consecutive nights subjects received 3 days off and conditions were reversed for 4 more consecutive nights. Tones started at 45dB and, in the absence of a response, increased 10dB every 10 seconds up to 95dB. Control subjects (N = 10) did not receive tones. The absolute number of arousals to tones was greater but the percentage of arousals was lower under the 4-min condition. Full awakenings occurred infrequently. Probability of making a breathing response remained high across days for both fragmentation conditions, but latency to respond was shorter and probability higher under the 8-min condition. Sleep fragmentation, whether “frequent” (4-min) or “infrequent” (8-min), did not induce greater daytime sleepiness than did the nonfragmentation control condition, and sleepiness did not differ between the two experimental conditions. Implications for developing behavioral techniques for treating sleep-related breathing disorders are discussed.     

Adverse childhood experiences associated with sleep in primary insomnia

The objectives were to explore the association between self-reported adverse childhood experiences (ACE) and sleep in adults suffering from primary insomnia and to examine the impact of presleep stress on this relationship. Fifty-nine patients with primary insomnia, aged 21-55 years, were administered the Childhood Trauma Questionnaire (CTQ) and then divided into two groups according to the achieved scores: with moderate/severe or low/no reports of ACE. The participants spent three consecutive nights in the sleep laboratory in order to record polysomnographic and actigraphic sleep parameters. A stress induction technique was administered by activating negative autobiographical memories immediately before sleep in the second or third night. Results show that 46% of the insomniac patients reported moderate to severe ACE. This group exhibited a significantly greater number of awakenings and more movement arousals compared to patients with low or no reports of ACE. Actigraphic data also indicated more disturbed sleep and increased nocturnal activity for the high-ACE group. On the other hand, no specific group differences were found with regard to stress condition. The results support the assumption that it is possible to identify a subgroup among patients with primary insomnia who has experienced severe maltreatment in childhood and adolescence. This subgroup appears to differ in several sleep parameters, indicating a more disturbed sleep compared to primary insomniacs with low or no reports of ACE. With regard to sleep-disturbing nightly patterns of arousal, parallels between individuals with high ACE and trauma victims as well as post-traumatic stress disorder-patients suggest themselves.     

Exploring the impact of experimental sleep restriction and sleep deprivation on subjectively perceived sleep parameters

We aimed to investigate the effect of increased sleep pressure and shortened sleep duration on subjective sleep perception in relation to electroencephalographic sleep measures. We analyzed the data from a study in which 14 healthy male volunteers had completed a baseline assessment with 8 hr time in bed, a sleep deprivation (40 hr of wakefulness) and a sleep restriction protocol with 5 hr time in bed during 7 nights. In this work, we assessed perception index, derived through dividing the subjectively perceived total sleep time, wake after sleep onset and sleep latency duration by the objectively measured one at each condition. We found that total sleep time was subjectively underestimated at baseline and shifted towards overestimation during sleep restriction and after deprivation. This change in accuracy of subjective estimates was not associated with any changes in sleep architecture or sleep depth. Wake after sleep onset was significantly underestimated only during sleep restriction. Sleep latency was always overestimated subjectively without any significant change in this misperception across conditions. When comparing accuracy of subjective and actimetry estimates, subjective estimates regarding total sleep time and wake after sleep onset deviated less from electroencephalography derived measures during sleep restriction and after deprivation. We conclude that self‐assessments and actimetry data of patients with chronic sleep restriction should be interpreted cautiously. The subjectively decreased perception of wake after sleep onset could lead to overestimated sleep efficiency in such individuals, whereas the underestimation of sleep time and overestimation of wake after sleep onset by actimetry could lead to further underestimated sleep duration.