Increased production of evoked and spontaneous K-complexes following a night of fragmented sleep

STUDY OBJECTIVES: To determine whether K-complex production is better interpreted as being an arousal response or reflective of a sleep protective micro-state. DESIGN: A 3-night study--night 1 as a baseline night, night 2 as a sleep fragmentation night, followed immediately by night 3 as a recovery night. On nights 1 and 3, approximately 400 auditory stimuli were presented during nonREM sleep in the first two sleep cycles, using stimulus parameters previously found to be optimal for K-complex production. SETTING: The sleep research laboratory at the University of Melbourne. PARTICIPANTS: Six young healthy subjects (3 female). INTERVENTIONS: One night of sleep fragmentation. Ten-second auditory tones of up to 110 dB were presented throughout the entire night at approximately 1-minute intervals. MEASUREMENTS AND RESULTS: Sleep drive was increased on the recovery night, as indicated by increased amounts of slow wave sleep, increased sleep efficiency, and a reduction in stimulus-related alpha activity. The incidence of both evoked and spontaneous K-complexes increased significantly on the recovery night. When K-complex trials were averaged, neither N550 (Fz) amplitude nor latency differed between the 2 nights. When vertex sharp waves were averaged, N350 (Cz) amplitude was increased significantly on the recovery night. CONCLUSIONS: The increase in K-complex frequency together with the decrease seen in stimulus-related alpha activity supports the view that they reflect a sleep maintenance, rather than an arousal, response.     

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.     

The relationship between frequency of rapid eye movements in REM sleep and SWS rebound

Previous studies have shown a decrease in rapid eye movement (REM) frequency during desynchronized sleep in recovery nights following total or partial sleep deprivation. This effect has been ascribed to an increase in sleep need or sleep depth consequent to sleep length manipulations. The aims of this study were to assess REM frequency variations in the recovery night after two consecutive nights of selective slow-wave sleep (SWS) deprivation, and to evaluate the relationships between REM frequency and SWS amount and auditory arousal thresholds (AAT), as an independent index of sleep depth. Ten normal males slept for six consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation and one recovery night. SWS deprivation allowed us to set the SWS amount during both deprivation nights close to zero, without any shortening of total sleep time. In the ensuing recovery night a significant SWS rebound was found, accompanied by an increase in AAT. In addition, REM frequency decreased significantly compared with baseline. This effect cannot be attributed to a variation in prior sleep duration, since there was no sleep loss during the selective SWS deprivation nights. Stepwise regression also showed that the decrease in REM frequency is not correlated with the increase in AAT, the traditional index of sleep depth, but is correlated with SWS rebound.     

Hyperarousal captured in increased number of arousal events during pre‐REM periods in individuals with frequent nightmares

The aim of this study was to investigate hyperarousal in individuals with frequent nightmares (NM participants) by calculating arousal events during nocturnal sleep. We hypothesized an increased number of arousals in NM participants compared with controls, especially during those periods where the probability of spontaneous arousal occurrence is already high, such as non‐rapid eye movement to rapid eye movement transitions (pre‐rapid eye movement periods). Twenty‐two NM participants and 23 control participants spent two consecutive nights in our sleep laboratory, monitored by polysomnography. Arousal number and arousal length were calculated only for the second night, for 10 min before rapid eye movement (pre‐rapid eye movement) and 10 min after rapid eye movement (post‐rapid eye movement) periods, as well as non‐rapid eye movement and rapid eye movement phases separately. Repeated‐measures ANOVA model testing revealed significant Group (NM participants, controls) × Phase (pre‐rapid eye movement, post‐rapid eye movement) interaction in case of the number of arousals. Furthermore, post hoc analysis showed a significantly increased number of arousals during pre‐rapid eye movement periods in NM participants, compared with controls, a difference that disappeared in post‐rapid eye movement periods. We propose that focusing the analyses of arousals specifically on state transitory periods offers a unique perspective into the fragile balance between the sleep‐promoting and arousal systems. This outlook revealed an increased number of arousals in NM participants, reflecting hyperarousal during pre‐rapid eye movement periods.     

Waking quantitative electroencephalogram and auditory event-related potentials following experimentally induced sleep fragmentation

STUDY OBJECTIVES: Experimental sleep fragmentation involves inducing arousals by administering intrusive auditory stimuli throughout the night. It is intended to model the frequent and periodic disruption experienced in common sleep disorders. Sleep fragmentation leads to daytime sleepiness, although evidence of performance impairment has been inconsistent. The purpose of this study was to investigate brain physiology associated with this level of sleep disruption. Specifically, quantitative analysis of electroencephalography was carried out, and auditory event-related potentials were recorded during daytime performance assessment following sleep fragmentation in good sleepers. DESIGN: Participants spent 4 consecutive 24-hour periods in the laboratory. On nights 2 and 3, sleep was fragmented using auditory stimuli that were delivered with increasing intensity until an arousal was noted. This design aimed to investigate the cumulative effects of sleep fragmentation on daytime functioning. SETTING: Data were collected in a sleep research laboratory during a 96-hour protocol. PARTICIPANTS: Eight healthy adults (mean age = 33.25) with no sleep complaints. MEASUREMENTS AND RESULTS: During the day, participants performed a 40-minute computerized test battery at 2-hour intervals (9:00 am -7:00 pm). The battery was presented in a fixed order and included measures of mood, sleepiness, reaction time, and serial addition or subtraction. Results indicated that subjective sleepiness and mood were impaired following sleep-fragmentation nights, compared to both baseline and recovery conditions. No performance deficits were apparent. The alpha:theta ratio, reflecting relative slowing of the electroencephalogram, was dramatically reduced following the second night of sleep fragmentation. Reductions in N1 amplitude of the event-related potentials indicated that attention was impaired with respect to early encoding processes following sleep fragmentation. CONCLUSIONS: Electroencephalographic and event-related potentials data illustrate impairment in information-processing capabilities associated with reduced arousal elicited by experimental sleep fragmentation. This subtle degree of sleep disruption, where total sleep time is not reduced, leads to sustained impairment in alertness and attention.     

Relationship of slow and rapid EEG components of CAP to ASDA arousals in normal sleep.

STUDY OBJECTIVES: Besides arousals (according to the ASDA definition), sleep contains also K-complexes and delta bursts which, in spite of their sleep-like features, are endowed with activating effects on autonomic functions. The link between phasic delta activities and enhancement of vegetative functions indicates the possibility of physiological activation without sleep disruption (i.e., arousal without awakening). A functional connection seems to include slow (K-complexes and delta bursts) and rapid (arousals) EEG events within the comprehensive term of activating complexes. CAP (cyclic alternating pattern) is the spontaneous EEG rhythm that ties both slow and rapid activating complexes together during NREM sleep. The present study aims at exploring the relationship between arousals and CAP components in a selected sample of healthy sleepers. DESIGN: Polysomnographic analysis according to the scoring rules for sleep stages and arousals. CAP analysis included also tabulation of subtypes A1 (slow EEG activating complexes), A2 and A3 (activating complexes with fast EEG components). SETTING: 40 sleep-lab accomplished recordings. PARTICIPANTS: Healthy subjects belonging to a wide age range (38 +/- 20 yrs.). INTERVENTIONS: N/A. MEASUREMENT AND RESULTS: Of all the arousals occurring in NREM sleep, 87% were inserted within CAP. Subtypes A2 and A3 of CAP corresponded strikingly with arousals (r=0.843; p<0.0001), while no statistical relationship emerged when arousals were matched with subtypes A1 of CAP. Subtypes A1 instead correlated positively with the percentages of deep sleep (r=0.366; p<0.02). CONCLUSIONS: The CAP subtype classification encompasses both the process of sleep maintenance (subtypes A1) and sleep fragmentation (subtypes A2 and A3), and provides a periodicity dimension to the activating events of NREM sleep.     

The effect of arousals during sleep onset on estimates of sleep onset latency

It is well established that insomniacs overestimate sleep-onset latency. Furthermore, there is evidence that brief arousals from sleep may occur more frequently in insomnia. This study examined the hypothesis that brief arousals from sleep influence the perception of sleep-onset latency. An average of four sleep onsets was obtained from each of 20 normal subjects on each of two nonconsecutive, counterbalanced, experimental nights. The experimental nights consisted of a control night (control condition) and a condition in which a moderate respiratory load was applied to increase the frequency of microarousals during sleep onset (mask condition). Subjective estimation of sleep-onset latency and indices of sleep quality were assessed by self-report inventory. Objective measures of sleep-onset latency and microarousals were assessed using polysomnography. Results showed that sleep-onset latency estimates were longer in the mask condition than in the control condition, an effect not reflected in objective sleep-stage scoring of sleep-onset latency. Furthermore, an increase in the frequency of brief arousals from sleep was detected in the mask condition, and this is a possible source for the sleep-onset latency increase perceived by the subjects. Findings are consistent with the concept of a physiological basis for sleep misperception in insomnia.     

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

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

Effects of two nights sleep deprivation and two nights recovery sleep on response inhibition

This study examined the effects of two nights of total sleep deprivation (TSD) and two nights of recovery sleep on response inhibition. Thirty-eight young, healthy adults performed a Go-NoGo task at 14 : 00 after: (1) a normal night of sleep; (2) each of two consecutive nights of TSD; and (3) each of two consecutive nights of recovery sleep; they also performed the task at 05 : 00 during the first night of sleep deprivation. We hypothesized that TSD would lead to an impaired ability to withhold a response that would be reversed with recovery sleep. Subjects did experience a significant increase in false positive responses throughout all of TSD, errors of omission (i.e. missed 'go' targets) were not significant until after the second night of TSD. Both components (withholding a response and automatic responding) of the task returned to baseline levels after one night of recovery sleep. These data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.     

The nature of arousal in sleep

The role of arousals in sleep is gaining interest among both basic researchers and clinicians. In the last 20 years increasing evidence shows that arousals are deeply involved in the pathophysiology of sleep disorders. The nature of arousals in sleep is still a matter of debate. According to the conceptual framework of the American Sleep Disorders Association criteria, arousals are a marker of sleep disruption representing a detrimental and harmful feature for sleep. In contrast, our view indicates arousals as elements weaved into the texture of sleep taking part in the regulation of the sleep process. In addition, the concept of micro-arousal (MA) has been extended, incorporating, besides the classical low-voltage fast-rhythm electroencephalographic (EEG) arousals, high-amplitude EEG bursts, be they like delta-like or K-complexes, which reflects a special kind of arousal process, mobilizing parallely antiarousal swings. In physiologic conditions, the slow and fast MA are not randomly scattered but appear structurally distributed within sleep representing state-specific arousal responses. MA preceded by slow waves occurs more frequently across the descending part of sleep cycles and in the first cycles, while the traditional fast type of arousals across the ascending slope of cycles prevails during the last third of sleep. The uniform arousal characteristics of these two types of MAs is supported by the finding that different MAs are associated with an increasing magnitude of vegetative activation ranging hierarchically from the weaker slow EEG types (coupled with mild autonomic activation) to the stronger rapid EEG types (coupled with a vigorous autonomic activation). Finally, it has been ascertained that MA are not isolated events but are basically endowed with a periodic nature expressed in non-rapid eye movement (NREM) sleep by the cyclic alternating pattern (CAP). Understanding the role of arousals and CAP and the relationship between physiologic and pathologic MA can shed light on the adaptive properties of the sleeping brain and provide insight into the pathomechanisms of sleep disturbances. Functional significance of arousal in sleep, and particularly in NREM sleep, is to ensure the reversibility of sleep, without which it would be identical to coma. Arousals may connect the sleeper with the surrounding world maintaining the selection of relevant incoming information and adapting the organism to the dangers and demands of the outer world. In this dynamic perspective, ongoing phasic events carry on the one hand arousal influences and on the other elements of information processing. The other function of arousals is tailoring the more or less stereotyped endogenously determined sleep process driven by chemical influences according to internal and external demands. In this perspective, arousals shape the individual course of night sleep as a variation of the sleep program.     

Phosphorous31 magnetic resonance spectroscopy after total sleep deprivation in healthy adult men

STUDY OBJECTIVES: To investigate chemical changes in the brains of healthy adults after sleep deprivation and recovery sleep, using phosphorous magnetic resonance spectroscopy. DESIGN: Three consecutive nights (baseline, sleep deprivation, recovery) were spent in the laboratory. Objective sleep measures were assessed on the baseline and recovery nights using polysomnography. Phosphorous magnetic resonance spectroscopy scans took place beginning at 7 am to 8 am on the morning after each of the 3 nights. SETTING: Sleep laboratory in a private psychiatric teaching hospital. PARTICIPANTS: Eleven healthy young men. INTERVENTIONS: Following a baseline night of sleep, subjects underwent a night of total sleep deprivation, which involved supervision to ensure the absence of sleep but was not polysomnographically monitored. MEASUREMENTS AND RESULTS: No significant changes in any measure of brain chemistry were observed the morning after a night of total sleep deprivation. However, after the recovery night, significant increases in total and beta-nucleoside triphosphate and decreases in phospholipid catabolism, measured by an increase in the concentration of glycerylphosphorylcholine, were observed. Chemical changes paralleled some changes in objective sleep measures. CONCLUSIONS: Significant chemical changes in the brain were observed following recovery sleep after 1 night of total sleep deprivation. The specific process underlying these changes is unclear due to the large brain region sampled in this exploratory study, but changes may reflect sleep inertia or some aspect of the homeostatic sleep mechanism that underlies the depletion and restoration of sleep. Phosphorous magnetic resonance spectroscopy is a technique that may be of value in further exploration of such sleep-wake functions.     

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

We evaluated the effects of selective slow-wave sleep (SWS) deprivation and time-of-night factors on cognitive performance upon awakening. Ten normal men slept for 6 consecutive nights in the laboratory: 1 adaptation, 2 baseline, 2 selective SWS deprivation, and 1 recovery night. Cognitive performance was assessed by means of a Descending Subtraction Task after 2, 5, and 7.5 h of sleep. There was an almost complete selective SWS suppression during both deprivation nights, and a significant SWS rebound during the recovery sleep. Regarding cognitive performance, a progressive linear decrease of sleep inertia upon successive awakenings was found during all experimental nights except for the recovery night. In addition, a significant decrease of sleep inertia was observed upon the morning awakening of the second deprivation night for the measure of performance speed, and a significant increase of sleep inertia upon the morning awakening of the recovery night for the measure of performance accuracy. The results show that cognitive performance upon awakening is adversely affected by sleep depth and that, during the sleep-wake transition, cognitive performance accuracy is more impaired than performance speed.     

Acute cardiovascular responses to arousal from non-REM sleep during normoxia and hypoxia.

STUDY OBJECTIVES: There is uncertainty concerning the relative contribution of arousal, chemoreceptor stimulation, and their potentially interactive effects, to the acute cardiovascular changes observed during sleep in patients with sleep-disordered breathing. The purpose of this study was to compare cardiovascular responses (heart rate, skin blood flow, and pulse transit time, a non-invasive measure of arterial wall stiffness) to auditory induced arousal from stage 2 sleep under conditions of normoxia and overnight mild hypoxia. DESIGN: Randomised crossover. SETTING: Sleep Disorders Unit in a 270-bed teaching hospital. PARTICIPANTS: Eleven healthy male subjects. INTERVENTIONS: Subjects slept wearing a facemask and breathed room air (one night; SaO2 approximately 98%) or an hypoxic gas mixture (two nights; SaO2 approximately 92%). Once in stage 2 sleep, subjects were administered one of 10 auditory tones (500 Hz, range 54-90 dB, 5-sec duration) via earphones or a sham tone (recording with no tone). MEASUREMENTS AND RESULTS: Cardiovascular responses were examined beat-by-beat for 20 seconds before and 30 seconds after auditory tones associated with arousals (3-10 second EEG changes) and after sham tones. Sleep efficiency and the percentage of sleep spent in each stage were not different between hypoxia and normoxia nights. Baseline heart rate was elevated on hypoxia nights compared with normoxia nights (59.5+/-1.7 vs. 54.4+/-1.6 b x min(-1), p=0.007). Heart rate, pulse transit time, and skin blood flow showed significant changes after arousal consistent with rapid parasympathetic withdrawal and sympathetic nervous system activation. No changes were observed after sham tones. There were no differences in time course or magnitude of cardiovascular responses between hypoxia and normoxia nights. CONCLUSIONS: We conclude that while mild hypoxia stimulates autonomic activity it does not augment the cardiovascular response to arousal from stage 2 sleep in normal subjects.     

Recovery sleep following different visual conditions during total sleep deprivation in man.

The findings of visual impairment during total sleep deprivation were used as a basis for a possible link between vision and sleep. It was proposed that the level of visual load imposed during sleep deprivation was an important variable, and would have a substantial effect upon recovery sleep. Six young male subjects underwent two conditions of 64 h of sleep deprivation on separate occasions. One condition incorporated a high visual load, and the other a low load. Exercise and sound were balanced. All night sleep EEGs were taken for two baseline nights, and also for two recovery nights following each condition. There was a significant increase of stage 4 on all recovery nights and a REM rebound on the second recovery night. SWS, particularly stage 4, TST and REM density, were significantly greater following the high load. Implications of these findings for sleep theories and for sleep deprivation research are discussed.     

CNS arousal and neurobehavioral performance in a short-term sleep restriction paradigm

Few studies have investigated waking electrophysiological measures of arousal during sleep restriction. This study examined electroencephalogram (EEG) activity and performance during a 96-hour laboratory protocol where participants slept a baseline night (8 h), were randomly assigned to 3-, 5-, or 8-hour sleep groups for the next two nights sleep restriction (SR1, SR2), and then slept a recovery night (8 h). There were dose-dependent deficits on measures of mood, sleepiness, and reaction time that were apparent during this short-term bout of sleep restriction. The ratio of alpha to theta EEG recorded at rest indicated dose-dependent changes in CNS arousal. At 9:00 hours, both the 3- and 5-hour groups showed EEG slowing (sleepiness) during restriction, with the 3-hour group exhibiting greater deficits. Later in the day at 13:00 hours, the 5-hour group no longer exhibited EEG slowing, but the extent of slowing was more widespread across the scalp for the 3-hour group. High-frequency EEG, a measure of effort, was greater on the mornings following sleep restriction. The 5-hour group had increased beta EEG at central-parietal sites following both nights of restriction, whereas the 3-hour group had increased beta and gamma EEG at occipital regions following the first night only. Short-term sleep restriction leads to deficits in performance as well as EEG slowing that correspond to the amount and duration of sleep loss. High-frequency EEG may be a marker of effort or compensation.     

Nightmares do result in psychophysiological arousal: A multimeasure ambulatory assessment study

Individuals who frequently experience nightmares report compromised sleep quality, poor daytime mood, and functioning. Previous research has aimed at linking these impairments with altered sleep architecture, but results were inconclusive. One plausible explanation is that only a few studies recorded markers of autonomic nervous system activity. For the first time, this study collected such markers under ecologically valid conditions with ambulatory assessment. In 19 individuals with frequent nightmares (≥1 nightmare/week) and 19 healthy control participants (<1 nightmare/month), measures indicating autonomic activation (heart rate, heart rate variability, respiration cycle length, electrodermal fluctuations, EEG arousals, saliva cortisol, REM density) were collected while applying ambulatory polysomnographic assessment during 3 consecutive nights. When nightmare participants reported a nightmare, we analyzed the last 5 min of REM sleep before awakening and compared these data to their non‐nightmares as well as to the dream episodes of control participants. Overall, there were no general differences in autonomic activation of nightmare sufferers compared to control participants. However, when nightmare participants experienced nightmares, autonomic activation was markedly increased compared to their own non‐nightmares and, to some extent, to control participant’s dreams. Significant intraindividual differences were found for all autonomic measures except in participant’s EEG arousals and cortisol levels. Group differences were found in EEG arousals and heart rate. In conclusion, ambulatory polysomnography demonstrates that nightmares are accompanied by increased autonomic activation. Results support the notion of impaired self‐reported sleep quality caused by one’s autonomic response rather than altered sleep pattern.     

Spontaneous arousability in prone and supine position in healthy infants

STUDY OBJECTIVE: Compared with control infants, those who will be future victims of sudden infant death syndrome (SIDS) show a decreased arousability during sleep, with fewer cortical arousals and more-frequent subcortical activations. These findings suggest an incomplete arousal process in victims of SIDS. Prone sleep position, a major risk factor for SIDS, has been reported to reduce arousal responses during sleep. The present study was undertaken to evaluate whether the prone sleep position impairs the arousal process in healthy infants. METHODS: Twenty-four healthy infants were studied polygraphically during 1 night; 12 infants regularly slept supine and 12 infants regularly slept prone. Infants were matched for sex, gestational age, and age at recording. Arousals were differentiated into subcortical activations or cortical arousals, according to the presence of autonomic and/or electroencephalographic changes. Frequencies of subcortical activations and cortical arousals were compared in the prone- and the supine-sleeping infants. RESULTS: Compared with supine sleepers, prone sleepers had significantly fewer cortical arousals during rapid eye movement (REM) sleep (p = .043). There were no significant differences in cortical arousals between the 2 groups during non-REM sleep. No significant differences were seen in the frequencies of subcortical activations during both REM and non-REM sleep between supine and prone sleepers. The ratio of cortical arousal to subcortical activation showed no significant differences between the prone and the supine sleepers. CONCLUSIONS: Prone sleep position decreased the frequency of cortical arousals but did not change the frequency of subcortical activations, as has been previously found in SIDS victims. These results suggest specific pathways for impairment of the arousal process in SIDS victims.     

Interaction of REM Deprivation and Stage 4 Deprivation With Total Sleep Loss: Experiment 2

To determine whether prior deprivation of stage REM or stage 4 sleep would potentiate the effects of total sleep loss, 7 young adult males were denied REM sleep and 7 were denied stage 4 sleep for 3 nights before 1 night of total sleep loss. Measures of autonomic and EEG activity, mood, anxiety, Rorschach CET and on several performance tasks were obtained during baseline, following stage deprivation, total sleep loss, and during recovery. There were no marked changes in any area following 3 nights of stage REM and stage 4 deprivation. The changes following total sleep loss were similar for both groups. Prior deprivation of stage REM or stage 4 did not potentiate sleep loss effects. Ss who had no stage deprivation prior to 1 night of sleep loss had more impairment following sleep loss than did the Ss of this study.     

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.     

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.