Effects of pre-sleep simulated on-call instructions on subsequent sleep

Nightly interventions, prevalent to on-call situations, can have negative consequences for those involved. We investigated if intervention-free-on-call-nights would also mean disturbance-free-sleep for people on-call. 16 healthy sleepers spent three nights in the laboratory: after a habituation night, reference and on-call night were counterbalanced. Subjects were instructed to react to a sound, presented at unpredictable moments during the night. Participants were unaware of the fact that the sound would never be presented. These vigilance instructions resulted in more subjective wake after sleep onset (WASO), lower subjective sleep efficiency and significantly lower experienced sleep quality. Objectively, a longer sleep onset, an increased amount of WASO and significantly lower sleep efficiency were observed. During deep sleep, significantly more beta activity was recorded. Apart from real nightly interventions increased vigilance during the night causes sleep to be less efficient and less qualitative as shown by an increase in wake-activity and a distorted sleep perception.     

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.     

The exploratory power of sleep effort,dysfunctional beliefs and arousal for insomnia severity and polysomnography‐determined sleep

Differences between subjective sleep perception and sleep determined by polysomnography (PSG) are prevalent, particularly in patients with primary insomnia, indicating that the two measures are partially independent. To identify individualized treatment strategies, it is important to understand the potentially different mechanisms influencing subjective and PSG‐determined sleep. The aim of this study was to investigate to what extent three major components of insomnia models, i.e. sleep effort, dysfunctional beliefs and attitudes about sleep, and presleep arousal, are associated with subjective insomnia severity and PSG‐ determined sleep. A sample of 47 patients with primary insomnia according to DSM‐IV criteria and 52 good sleeper controls underwent 2 nights of PSG and completed the Glasgow Sleep Effort Scale, the Dysfunctional Beliefs and Attitudes about Sleep Scale, the Pre‐Sleep Arousal Scale and the Insomnia Severity Index. Regression analyses were conducted to investigate the impact of the three predictors on subjective insomnia severity and PSG‐ determined total sleep time. All analyses were adjusted for age, gender, depressive symptoms and group status. The results showed that subjective insomnia severity was associated positively with sleep effort. PSG‐determined total sleep time was associated negatively with somatic presleep arousal and dysfunctional beliefs and attitudes about sleep. This pattern of results provides testable hypotheses for prospective studies on the impact of distinct cognitive and somatic variables on subjective insomnia severity and PSG‐determined total sleep time.     

Sleep microstructure around sleep onset differentiates major depressive insomnia from primary insomnia

In the present study we investigate whether alterations of sleep propensity or of wake propensity are implicated in sleep initiation disturbances encountered in major depressive insomnia and in primary insomnia. For this purpose, the time course of electroencephalogram (EEG) power density during the period preceding sleep onset and during the first non-rapid eye movement (REM) period was examined in three age and gender matched groups of 10 women and 11 men (healthy controls, primary insomniacs and depressive insomniacs). In contrast to healthy controls and depressive insomniacs, patients with primary insomnia did not experience a gradual decrease of their alpha and beta1 power during the sleep onset period and had a lower delta activity in the 5 min preceding sleep onset. Compared with the two other groups, depressive patients exhibit less dynamic changes in slow wave activity during the first non-REM period. The present results suggest that hyperarousal (high 'Process W') may mainly be implicated in the sleep initiation difficulties of primary insomniacs whereas the homeostatic sleep regulation process seems to be partially maintained. In our major depressed patients, the sleep initiation disturbances appeared to relate to a lower sleep pressure (low 'Process S') rather than to hyperarousal. This study supports the idea that different mechanisms are implicated in sleep disturbances experienced by primary insomniacs and major depressive insomniacs.     

Effect of cognitive arousal on sleep latency, somatic and cortical arousal following partial sleep deprivation

Emerging research has shown that sleepiness, defined as the tendency to fall asleep, is not only determined by sleep pressure and time of day, but also by physiological and cognitive arousal. In this study we evaluated (i) the impact of experimentally induced cognitive arousal on electroencephalogram (EEG) defined sleep latency, and subjective, somatic and cortical arousal, and (ii) whether experimentally induced cognitive arousal enhances performance on a driving simulator test. Twelve healthy sleepers each spent three nights and the following day in the sleep laboratory: an adaptation, a cognitive arousal and a neutral testing day. In the cognitive arousal condition, a visit of a television camera crew took place and subjects were asked to be interviewed. On each testing day, a 5-min heart rate recording, subjective sleepiness and arousal scales, Multiple Sleep Latency Test and a 25-min driving simulator task were scheduled three times at 2-h intervals. Experimentally induced cognitive arousal resulted in significant increases in objective sleep latency. Significantly elevated levels of subjective and somatic arousal--as indexed by a subjective arousal scale and heart rate--were also evidenced following cognitive arousal induction. A marginally significant trend for increased cortical arousal, measured by EEG beta activity, was also found. No effects were found on driving simulator performance. These findings support the concept of cognitive arousal as a significant component in determining sleep latency. In addition, it was illustrated that cognitively induced arousal can provoke increases in somatic and possibly even cortical arousal in normal sleepers. However, this was not accompanied by an enhanced ability to perform adequately on a driving simulator test.     

A pathogenic cycle between insomnia and cognitive arousal fuels perinatal depression: exploring the roles of nocturnal cognitive arousal and perinatal-focused rumination

Study ObjectivesDepression is among the most prevalent perinatal complications, yet modifiable risk factors remain elusive. Over half of perinatal women endorse clinical insomnia symptoms, which are etiologically implicated in depression in nonperinatal samples. Yet, prospective data on perinatal insomnia and depression are mixed. We sought to clarify temporal associations of insomnia and depression during peripartum, and to investigate cognitive arousal as a potential mechanism facilitating this relationship.MethodsSeventy pregnant women completed sociodemographic information and baseline sleep and mood symptoms between gestational weeks 25 and 30. Beginning at gestational week 30, participants completed 17 weekly online surveys assessing insomnia, depression, and three cognitive arousal indices (nocturnal cognitive arousal, perseverative thinking, and perinatal-focused rumination). Mixed effects models were conducted to test hypotheses.ResultsWomen were at risk for depression when experiencing insomnia (odds ratio [OR] = 2.36, 95% confidence interval [CI] = 1.28 to 4.35), nocturnal cognitive arousal (OR = 3.05, 95% CI = 1.60 to 5.79), perinatal-focused rumination (OR = 2.05, 95% CI = 1.11 to 3.79), and perseverative thinking (OR = 7.48, 95% CI = 3.90 to 14.32). Prospective analyses revealed bidirectional effects between insomnia and cognitive arousal, and both predicted future depression. Nocturnal cognitive arousal mediated 23–43% of the effect of insomnia on depression. Insomnia mediated 12%–18% of the effect of nocturnal cognitive arousal on depression. A similar pattern was observed with perinatal-focused rumination. Depression did not predict insomnia.ConclusionNocturnal cognitive arousal, including ruminating on perinatal concerns while trying to fall asleep, fuels insomnia. In turn, lying awake at night provides an opportunity for nocturnal cognitive arousal. This cycle feeds perinatal depression. Daytime cognitive arousal may indirectly disrupt sleep as perseverating during the day persists into the night.     

Intrinsic dreams are not produced without REM sleep mechanisms: evidence through elicitation of sleep onset REM periods

The hypothesis that there is a strict relationship between dreams and a specific rapid eye movement (REM) sleep mechanism is controversial. Many researchers have recently denied this relationship, yet none of their studies have simultaneously controlled both sleep length and depth prior to non-REM (NREM) and REM sleep awakenings, due to the natural rigid order of the NREM--REM sleep cycle. The failure to control sleep length and depth prior to arousal has confounded interpretations of the REM-dreams relationship. We have hypothesised that different physiological mechanisms underlie dreaming during REM and NREM sleep, based on recent findings concerning the specificity of REM sleep for cognitive function. Using the Sleep Interruption Technique, we elicited sleep onset REM periods (SOREMP) from 13 normal subjects to collect SOREMP and sleep onset NREM (NREMP) dreams without the confounds described above. Regression analyses showed that SOREMP dream occurrences were significantly related to the amount of REM sleep, while NREMP dream occurrences were related to arousals from NREM sleep. Dream properties evaluated using the Dream Property Scale showed qualitative differences between SOREMP and NREMP dream reports. These results support our hypothesis and we have concluded that although 'dreaming' may occur during both REM and NREM periods as previous researchers have suggested, the dreams obtained from these distinct periods differ significantly in their quantitative and qualitative aspects and are likely to be produced by different mechanisms.     

Sleep onset and cardiovascular activity in primary insomnia

The transition from wakefulness to sleep is characterized typically by a shift from sympathetic to parasympathetic regulation. Physiological functions, depending on the neurovegetative system, decrease overall. Previous studies have shown cardiovascular and electroencephalographic hyperactivity during wakefulness and sleep in insomniacs compared with normal sleepers, but there is very little evidence of this in the process of sleep onset. The purpose of this study was to compare cardiovascular and autonomic responses before and after falling asleep in eight insomniacs (who met DSM‐IV criteria for primary insomnia) and eight normal sleepers. Non‐invasive measures of heart rate (HR), stroke volume (SV), cardiac output (CO) and pre‐ejection period (PEP) were collected by impedance cardiography during a night of polysomnographic recording. Frequency domain measures [low‐frequency (LF), high‐frequency (HF)] of heart rate variability (HRV) were also estimated. Decrements in HR and CO and increases in SV and HF normalized units (n.u.) were found in both groups after sleep onset compared with wakefulness. Conversely, PEP (related inversely to sympathetic β‐adrenergic activity) showed increases after sleep onset in controls, but remained unchanged in insomniacs. PEP was also significantly lower in insomniacs than in normal sleepers in both conditions. These data suggest that, whereas normal sleepers follow the expected progressive autonomic drop, constant sympathetic hyperactivation is detected in insomniacs. These results support the aetiological hypothesis of physiological hyperarousal underlying primary insomnia.     

Slow horizontal eye movement at human sleep onset

Slow eye movement (SEM) at human sleep onset has been studied as a function of EEG and behavioral state but has not been subjected to systematic physical measurement. This study counted the frequency of horizontal SEM and quantified its physical properties during hypnagogic EEG stages 3-8 (stage 1 sleep). SEM amplitudes, peak velocities, and durations were digitally measured. As in previous studies SEM occurred throughout stage 1 sleep, coinciding with all tonic states and with all phasic events that classically define stage 1. Within stage 1 the physical properties of SEM varied significantly. In hypnagogic stage 3, where EEG alpha dominates up to half of any 30-s epoch, the typical SEM was moderate in amplitude, slow, and short-lasting, and SEM peak velocity described a weak function of SEM amplitude. In stages 5 and 6 combined--characterized by a low-voltage delta-theta EEG, sustained alpha suppression, and no more than one vertex sharp wave (VSW) per 30-s epoch--SEM velocity was maximal, and described a strong function of amplitude. Despite low absolute velocities, stage 5/6 SEM could approximate saccade-like morphologies. In stages 7 and 8 combined, characterized by VSW bursts and incipient spindles or K complexes, SEM was maximal in amplitude and duration but not faster than SEM in stage 5/6. These properties of human SEM are discussed in relation to the anatomy and physiology of SEM in macaque.     

The influence of sleep onset on the diurnal variation in cardiac activity and cardiac control

Heart rate (HR), blood pressure (BP) and autonomic nervous system (ANS) activity vary diurnally, with a reduction in HR and BP, and a shift to vagal dominance during the dark phase. However, the cause of these changes, particularly the relative influence of sleep and circadian mechanisms, remains uncertain. The present study assessed the effect of sleep onset on HR, BP, high frequency (HF) component of heart rate variability (HRV), low frequency/high frequency (LF/HF) ratio and pre-ejection period (PEP). Sleep onset was dissociated from circadian influences by having subjects go to sleep at two different circadian phases, their normal time of sleep onset (normal sleep onset, NSO), and after a delay of 3 h (delayed sleep onset, DSO). The assumption was that changes caused by sleep onset would occur in association with sleep onset, irrespective of its timing, while circadian effects would have a consistent circadian phase and be independent of when sleep onset occurred. Thirteen and 17 subjects were run in the NSO and DSO conditions, respectively. Following a 1-h adaptation period, data collection began 2 h before subjects' normal time of sleep onset and continued until morning awakening. The lights were turned out after 2 h in the NSO condition and 5 h in the DSO condition. Subjects were required to maintain a supine position throughout the experimental sessions. The night-time decrease in HR was found to be due to both sleep onset and a circadian influence, with the circadian component being more prominent. In contrast, the fall in BP was largely due to a sleep onset effect. Increased vagal activity, as reflected in the HF component and a shift to vagal dominance in the LF/HF ratio, appeared to be primarily a function of the sleep system, while sympathetic activity, as assessed by PEP, reflected a circadian influence.     

Fragments of wake-like activity frame down-states of sleep slow oscillations in humans: New vistas for studying homeostatic processes during sleep

During NREM sleep cortical activity corresponding to EEG fast rhythms (FRs > 10 Hz) is interrupted by fragments of neural stillness (down-states), responsible for the negative peak within sleep slow oscillation (SSO). Researchers still debate whether the down-states spontaneously occur or need an initial overshoot in fluctuating activity. Herein, we studied temporally-isolated SSO in healthy subjects in order to identify two distinct EEG markers defining a putative initial up-state: i) a significant positive deflection and ii) an associated FR increase, before the negative peak.     

A pilot study of a novel smartphone application for the estimation of sleep onset

The aim of the study was to investigate the accuracy of Sleep On Cue: a novel iPhone application that uses behavioural responses to auditory stimuli to estimate sleep onset. Twelve young adults underwent polysomnography recording while simultaneously using Sleep On Cue. Participants completed as many sleep‐onset trials as possible within a 2‐h period following their normal bedtime. On each trial, participants were awoken by the app following behavioural sleep onset. Then, after a short break of wakefulness, commenced the next trial. There was a high degree of correspondence between polysomnography‐determined sleep onset and Sleep On Cue behavioural sleep onset, r = 0.79, P < 0.001. On average, Sleep On Cue overestimated sleep‐onset latency by 3.17 min (SD = 3.04). When polysomnography sleep onset was defined as the beginning of N2 sleep, the discrepancy was reduced considerably (M = 0.81, SD = 1.96). The discrepancy between polysomnography and Sleep On Cue varied between individuals, which was potentially due to variations in auditory stimulus intensity. Further research is required to determine whether modifications to the stimulus intensity and behavioural response could improve the accuracy of the app. Nonetheless, Sleep On Cue is a viable option for estimating sleep onset and may be used to administer Intensive Sleep Retraining or facilitate power naps in the home environment.     

fMRI differences between early and late stage-1 sleep

This study sought to test for differences in regional brain activity between stage-1 sleep immediately following wake and immediately preceding stage-2 sleep. Data were collected during daytime fMRI sessions with simultaneous EEG acquisition. A stage-1 interval was defined as follows: ≥30 s of wake, immediately followed by ≥60 s of continuous stage 1, immediately followed by ≥30 s of stage 2. We compared brain activity between the first 30 s of stage 1 (early stage 1), the last 30 s of stage 1 (late stage 1), and isolated wake. A conjunction analysis sorted each voxel into one of a series of mutually exclusive categories that represented the various possible combinations of a significant increase, decrease, or no difference among these three states. The initial dataset consisted of 14 healthy volunteers. A total of 22 sessions in these participants yielded six stage-1 intervals (from four participants) that met criteria for inclusion in the analysis. There were multiple clusters of significant voxels. Examples include changes in default-mode network areas where activity increased compared to wake only in early stage 1 and a bilateral change in the hippocampus where activity increased compared to wake only in late stage 1. These results suggest that activity in anatomically identifiable, volumetric brain regions exhibit differences during stage-1 sleep that would not have been detected with the EEG. These differences may also have specific relevance to understanding the process of sleep onset as well as the neural mechanisms of performance lapses during sleep deprivation.     

On arousal from sleep: time-frequency analysis

Time-frequency analysis of the heart rate variability during arousal from sleep, with and without EMG activation, coming from five obese healthy subjects was performed. Additionally, a comparative analysis of three time-frequency distributions, smooth pseudo Wigner–Ville (SPWVD), Choi–Williams (CWD) and Born–Jordan distribution (BJD) is presented in this study. SPWVD showed higher capacity for eliminating the cross terms independently of the signal. After applying Hilbert transformation to real signals BJD and CWD lost some important mathematic properties as marginals, on the contrary PSWVD remains unchanged. BJD showed results comparable with CWD. During arousal episodes, analogous energy distribution and spectral indexes were obtained by the three time-frequency representations. Arousals with chin activity presented stronger changes in RR intervals and LF (related to sympathetic activity) component, being statistically different with respect to arousal without chin activity, only around the period of maximum change in β activity on the EEG. These results suggest a more evident stress for the heart when an arousal is related to external muscular activity.     

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.     

Day-time melatonin administration: Effects on core temperature and sleep onset latency

Significant hypothermic and hypnotic effects have been reported for melatonin at a wide range of doses. It has been suggested that this decrease in core temperature (Tc) following melatonin administration may mediate the observed increase in sleepiness. To test this, melatonin was administered to young adults during the day, and the concurrent effects on Tc and sleep onset latency (SOL) were recorded. Sixteen healthy males received either a 5 mg oral formulation of melatonin or placebo at 14.00 hours. Core temperature was recorded continuously. Sleep onset latency to stage 1 (SOL1) and stage 2 (SOL2) were recorded using an hourly multiple sleep latency test (MSLT). Compared with placebo, melatonin significantly decreased Tc 1.5 h after administration for 6 h. Between 15.00 and 18.00 hours, the drop in Tc was associated with a concurrent decrease in SOL1 and SOL2. Following administration mean SOL1 and SOL2 were reduced by 40 and 25%, respectively. In this study, daytime melatonin administration produced a significant decrease in Tc with a corresponding decrease in SOL. Taken together, these data are not inconsistent with the suggestion that melatonin may facilitate sleep onset via a hypothermic effect. In addition, this study provides support for the idea that melatonin may play a role in regulating circadian and/or age-related variations in sleep/wake propensity. From a practical perspective, exogenous melatonin may be useful in the treatment of sleep disorders associated with increased nocturnal Tc.     

Changes in the scalp topography of event-related potentials and behavioral responses during the sleep onset period

Event-related potentials (ERPs) and behavioral responsiveness were investigated during the transition from wakefulness to sleep. Ten participants were presented with an auditory oddball task during repeated sleep onset periods. The EEG was recorded from 29 different scalp sites. A 1500-Hz tone pip was presented infrequently (p = .04) within a series of lower pitch 1000-Hz "standard" stimuli (p = .96). Participants were required to button press upon detection of the rare "target" stimulus. During wakefulness, almost all targets were detected. A large amplitude P300 was observed to these detected targets. This P300 was maximum over parietal areas of the scalp. During stage 1 sleep, subjects continued to respond on 47% of trials. The parietal P300 amplitude remained large to these detected targets. It was, however, much attenuated at frontal sites. When the participant failed to detect the target in either stage 1 or 2, no P300 was visible. P300 is thus associated with behavioral detection of the target stimulus, whether in wakefulness or stage 1 "sleep." Trials were also sorted by reaction time (RT), in which bins 1-3 represented increasingly long RT. In the waking state, P300 amplitude did not significantly vary across the different bins. Although mean RT latency varied by 512 ms from bin 1 to bin 3, P300 latency varied by only 25 ms. Differences in RT are thus probably due to response-related processes rather than stimulus classification time.     

EEG spectral power and cognitive performance during sleep inertia: the effect of normal sleep duration and partial sleep deprivation

Sleep inertia (SI) is a transient period occurring immediately after awakening, usually characterized by performance decrement. When sleep is sufficient, SI is moderate, and produces few or no deficit. When it is associated with prior sleep deprivation, SI shows dose-dependent negative effects on cognitive performance, especially when subjects have been awaken in slow wave sleep (SWS). In the present study, spectral analysis was applied during the last 10 min before and the first 10 min after awakening, and during 1 h after awakening while subjects performed the Stroop test. Seventeen subjects were divided into a Control group who slept 8 h, and a Sleep Deprived group who slept only 2 h. The results show that performance was normal in the Control group, whereas reaction time was increased during the first half hour and error level during the second half hour in the Sleep Deprived group. Spectral analysis applied on the waking EEG during the whole test session showed that alpha activity was increased in both groups, but theta power only in the Sleep Deprived group. There was a high positive correlation in sleep deprived subjects between delta power during the last 10 min of sleep and subsequent performance decrement in speed and accuracy. Comparison of individual records showed a high positive correlation between spectral power before and after awakening in the Control group (generally in the sense of an increased frequency band), but no correlation was found in the Sleep Deprived group who exhibited a rather disorganized pattern. We discuss these results in terms of incoherence in the EEG continuity during sleep offset after prior sleep loss, which could partly account for the performance decrement observed during SI in sleep deprived subjects.     

The dim light melatonin onset following fixed and free sleep schedules

The time at which the dim light melatonin onset (DLMO) occurs can be used to ensure the correct timing of light and/or melatonin administration in order to produce desired circadian phase shifts. Sometimes however, measuring the DLMO is not feasible. Here we determined if the DLMO was best estimated from fixed sleep times (based on habitual sleep times) or free (ad libitum) sleep times. Young healthy sleepers on fixed (n=60) or free (n=60) sleep schedules slept at home for 6 days. Sleep times were recorded with sleep logs verified with wrist actigraphy. Half-hourly saliva samples were then collected during a dim light phase assessment and were later assayed to determine the DLMO. We found that the DLMO was more highly correlated with sleep times in the free sleepers than in the fixed sleepers (DLMO versus wake time, r=0.70 and r=0.44, both P<0.05). The regression equation between wake time and the DLMO in the free sleepers predicted the DLMO in an independent sample of free sleepers (n=23) to within 1.5 h of the actual DLMO in 96% of cases. These results indicate that the DLMO can be readily estimated in people whose sleep times are minimally affected by work, class and family commitments. Further work is necessary to determine if the DLMO can be accurately estimated in people with greater work and family responsibilities that affect their sleep times, perhaps by using weekend wake times, and if this method will apply to the elderly and patients with circadian rhythm disorders.     

Clonidine has a paradoxical effect on cyclic arousal and sleep bruxism during NREM sleep

Study Objective:

Clonidine disrupts the NREM/REM sleep cycle and reduces the incidence of rhythmic masticatory muscle activity (RMMA) characteristic of sleep bruxism (SB). RMMA/SB is associated with brief and transient sleep arousals. This study investigates the effect of clonidine on the cyclic alternating pattern (CAP) in order to explore the role of cyclic arousal fluctuation in RMMA/SB.

Design:

Polysomnographic recordings from a pharmacological study.

Setting:

University sleep research laboratory.

Participants and Interventions:

Sixteen SB subjects received a single dose of clonidine or placebo at bedtime in a crossover design.

Measurements and Results:

Sleep variables and RMMA/SB index were evaluated. CAP was scored to assess arousal instability between sleep-maintaining processes (phase A1) and stronger arousal processes (phases A2 and A3). Paired t-tests, ANOVAs, and cross-correlations were performed. Under clonidine, CAP time, and particularly the number of A3 phases, increased (P ≤ 0.01). RMMA/SB onset was time correlated with phases A2 and A3 for both placebo and clonidine nights (P ≤ 0.004). However, under clonidine, this positive correlation began up to 40 min before the RMMA/SB episode.

Conclusions:

CAP phase A3 frequency increased under clonidine, but paradoxically, RMMA/SB decreased. RMMA/SB was associated with and facilitated in CAP phase A2 and A3 rhythms. However, SB generation could be influenced by other factors besides sleep arousal pressure. NREM/REM ultradian cyclic arousal fluctuations may be required for RMMA/SB onset.

Citation:

Carra MC; Macaluso GM; Rompré PH; Huynh N; Parrino L; Terzano MG; Lavigne GJ. Clonidine has a paradoxical effect on cyclic arousal and sleep bruxism during NREM sleep. SLEEP 2010;33(12):1711-1716.