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Study Objective: In healthy subjects, arousability to inspiratory resistive loading is greater during rapid eye movement (REM) sleep compared with non-REM (NREM) sleep but is poorest in REM sleep in patients with sleep apnea. We therefore examined the hypothesis that sleep fragmentation impairs arousability, especially from REM sleep., Design: Two blocks of 3 polysomnographies (separated by at least 1 week) were performed randomly. An inspiratory-loaded night followed either 2 undisturbed control nights (LN(C)) or 2 acoustically fragmented nights (LN(F)) SETTING: Sleep laboratory., Participants: Sixteen healthy men aged 20 to 29 years., Interventions: In both loaded nights, an inspiratory resistive load was added via a valved facemask every 2 minutes during sleep and turned off either when arousal occurred or after 2 minutes., Measurements and Results: During LN(F), arousability remained significantly greater in REM sleep (71% aroused within 2 minutes) compared with stage 2 (29%) or stage 3/4 (16%) sleep. After sleep fragmentation, arousability was decreased in stage 2 sleep (LN(F): 29%; LN(C): 38%; p < .05) and low in early REM sleep, increasing across the night (p < .01). In stage 3/4 sleep, neither an attenuation nor a change across the night was seen after sleep fragmentation., Conclusions: Mild sleep fragmentation is already sufficient to attenuate arousability in stage 2 sleep and to decrease arousability in early, compared with late, REM sleep. This means that sleep fragmentation affects the arousal response to increasing resistance and that the effects are different in stage 2 and REM sleep. The biologic reason for this increase in the arousal response in REM sleep across the night is not clear.

There are no visible electroencephalographic (EEG) changes at the termination of some apnoeas and hypopnoeas. This study tests the hypothesis that cortical activity fluctuates at apnoea/hypopnoea termination, despite the lack of visible changes. To detect these changes, EEG spectral analysis was performed and centred around the end of apnoeas/hypopnoeas in 15 sleepy patients. Ten second windows were applied and comparisons were conducted between the normalised power of the same frequency bands before and after termination of each apnoea/hypopnoea. Comparisons were performed within patients between apnoeas/hypopnoeas and periods of undisturbed sleep as well as between patients and healthy subjects during sleep. Normalised theta power (4-8 Hz) decreased significantly at apnoea/hypopnoea termination. No significant changes were found between consecutive periods of undisturbed sleep across the 15 patients. During nonrapid eye movement sleep, changes were detected irrespective of arousal visibility. During rapid eye movement sleep, nonarousal apnoeas/hypopnoeas were not accompanied by any significant spectral power changes. Theta power was significantly lower across patients compared to healthy subjects (p=0.03) and was correlated to the apnoea/hypopnoea index (rho=0.6, p=0.008). The authors conclude that electroencephalographic spectral analysis improves detection of changes at apnoea/hypopnoea termination. Further validation is needed to determine whether it improves correlation between nocturnal measures and daytime symptoms.

Sleep disruption and daytime sleepiness in obstructive sleep apnoea/hypopnoea syndrome (OSAHS) patients result from recurrent apnoeas/hypopnoeas and arousals from sleep. Around 30% of apnoeas/hypopnoeas are not terminated by visible cortical arousals. The current authors tested the hypotheses that arousal induction is linked to sleep stage, oxygen desaturation, event type, event duration and time of occurrence during the night. Fifteen patients with OSAHS of varying severity were studied and all their apnoeas/hypopnoeas were evaluated. Eight of 15 patients had apnoeas/hypopnoeas in all sleep stages, and all their 610 apnoeas/hypopnoeas were analysed in the between stages comparison; data from all 15 patients were included in other comparisons. Thirty-four per cent of apnoeas/hypopnoeas during slow wave sleep (SWS) were associated with arousal, significantly less than the 77% during nonrapid eye movement (NREM) 1 and 2 and 62% during rapid eye movement (REM) sleep. Arousal induction was not affected by oxygen desaturation, event type, duration or time of the night. The apnoeal/hypopnoea index was 39 x h(-1) in REM 1 and 2, significantly higher compared to 17 x h(-1) in REM or to 11 x h(-1) in SWS sleep. In conclusion, apnoeas/hypopnoeas in slow wave sleep are associated with fewer cortically apparent, visually detected arousals.

There have been relatively few robust studies of the effects of CPAP therapy on vigilance and daytime function. This article will use all known published and unpublished randomized clinical trials on this area. There is good evidence that CPAP helps subjective sleepiness, objective sleepiness, quality of life, mood and driving performance. However, CPAP does not appear to normalize objective sleepiness. Many of the improvements are directly related to the nightly use of CPAP. Recent data suggest that increasing CPAP usage improves outcomes.

Continuous positive airway pressure (CPAP) therapy improves daytime function in the sleep apnea/ hypopnea syndrome (SAHS) but it is unclear which patients benefit and what factors predict this improvement. To test the hypothesis that brief arousals from sleep predict improvements in daytime functioning with CPAP therapy, we prospectively studied 62 patients with polysomnography-defined SAHS. Each underwent daytime function assessments at baseline and after 6 mo of CPAP therapy to measure objective sleepiness, psychological well-being, quality of life, and cognitive performance. The microarousal frequency and AHI were poor predictors of improvements in daytime function with CPAP. Measures of hypoxemia predicted improvements in the mean sleep latency on the maintenance of wakefulness test, SAHS symptoms, quality of life, and reaction time, but such correlations were weak or moderate only explaining between 7% and 22% of variance. Significant relationships were found between CPAP use and improvements in self-ratings of daytime function. Results suggest that standard polysomnographic baseline variables are poor predictors of the response to CPAP therapy.

Patients with the sleep apnoea/hypopnoea syndrome (SAHS) have impaired daytime function with demonstrable sleepiness and impaired cognition. The hypothesis that brief arousals from sleep cause these daytime impairments was tested. One hundred and fifty patients with sleep disordered breathing were studied prospectively, comparing overnight polysomnography with daytime measures of objective sleepiness, psychological well-being and cognitive performance. Significant, but weak (r2<0.1), relationships were seen between several nocturnal measures (apnoea/hypopnoea index, arousals and desaturation variables) and daytime measures of quality of life, well-being, subjective sleepiness, symptoms and cognitive performance. The only significant relationship between nocturnal variables and objective sleepiness was a very weak correlation (r2<0.05) between the lowest oxygen saturation and mean maintenance of wakefulness test (MWT) result. The MWT was better correlated with daytime function than the multiple sleep latency test. This study shows a lack of strong relationships between conventional nocturnal measures and daytime function in patients with sleep disordered breathing.

Limited sleep study systems are increasingly being used to diagnose the sleep apnoea/hypopnoea syndrome, but validation is essential and detection of arousal's desirable. One such system (AutoSet) was validated on an event-by-event basis, and the hypothesis that sudden large breaths detected by this system mark arousal from sleep was also examined. Twenty consecutive patients (apnoea/hypopnoea index (AHI) 39+/-6 (SEM)) underwent polysomnography (PSG), which included real-time signals of AutoSet (Version 3.03) scored events. PSG respiratory events were defined using airflow and thoracoabdominal movement and AutoSet events using nasal pressure. All apnoeas were scored by both systems, but 41% more hypopnoeas were scored on PSG and these were clinically significant, with 78% ending in cortical arousal. Twenty per cent of apnoeas and hypopnoeas scored by the AutoSet occurred during wakefulness. Large breaths, defined as a two-thirds increase in ventilation, marked 77% of respiratory-associated but only 9% of spontaneous arousals. Large breaths also marked 48% of "autonomic" arousals following respiratory events without visible electroencephalographic changes. Twenty-seven per cent of large breaths occurred during wakefulness. This study shows that the AutoSet and the standard polysomnographic approach differ in their detection of hypopnoeas. The AutoSet underdetected hypopnoeas during sleep, but also included some hypopnoeas occurring during wakefulness. Detection of large breaths may potentially be useful for identifying respiratory arousals. Detection of periods of wakefulness may improve the accuracy of the system.

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 (rho=-0.30, P<0.01). There were weakly significant relationships between all three microarousal definitions (-0.24

As daytime deficits in sleep apnea/hypopnea syndrome (SAHS) correlate poorly with earlier definitions of arousals, we investigated the relationship between microarousals and sleepiness in 63 patients with SAHS. There was a poor correlation between mean sleep latency and microarousal frequency. To determine whether arousals not detected by current definitions could account for some of the residual variance in normal subjects we used sound to induce "arousals" that were detected by rises in blood pressure but produced no visible EEG change. Such autonomic arousals produced an increase in sleepiness. We conclude that arousals not scored currently on polysomnography may contribute to the sleepiness of patients with SAHS.

Patients with the sleep apnea/hypopnea syndrome suffer from impaired daytime function. This has been attributed to both sleep fragmentation and hypoxemia. To help understand which is casual, we studied the effects of sleep fragmentation alone on daytime function. Sixteen normal subjects were studied on two pairs of two nights. The first night of each pair was for acclimatization, and on the second the subject either slept undisturbed or had sleep fragmented with sound pulses every 2 min. Sound volume and duration was titrated to cause a return to theta or alpha rhythm on the EEG for at least 3 s. Study nights were followed by daytime testing of psychometric function and mood and by a multiple sleep latency test (MSLT) and a maintenance of wakefulness test (MWT). Total sleep time did not differ between study nights (400 +/- 20 SD min undisturbed, 396 +/- 24 min fragmented; p = 0.6). Fragmentation decreased sleep latency on both the MSLT (11 +/- 3, 7 +/- 2 min; p = 0.001) and the MWT (34 +/- 8, 24 +/- 10 min; p<0.001). Energetic arousal (22 +/- 4, 19 +/- 4; p = 0.005) and hedonic tone (29 +/- 4, 27 +/- 4; p = 0.05) decreased after fragmentation. Fragmentation impaired daytime function adjudged by the Trailmaking B (p = 0.05) and PASAT 4-s tests (p<0.03). One night of sleep fragmentation makes normal subjects sleepier during the day, impairs their subjective assessment of mood, and decreases mental flexibility and sustained attention.

Brief arousals are clinically important and increasingly scored during polysomnography. However, the frequency of arousals during routine polysomnography in the normal population is unknown. We performed overnight polysomnography in the 55 of 59 control subjects from a family practice list who were approached and agreed to undergo polysomnography. Awakenings were scored according to the criteria of Rechtschaffen and Kales and briefer arousals according to three different criteria, including the American Sleep Disorders Association (ASDA) definition. There was a mean of 4 [95% confidence interval (CI), 1-15) Rechtschaffen and Kales awakenings per hour, whereas the ASDA definition gave 21 (95% CI, 7-56) per hour slept. Arousal frequencies increased significantly (p < 0.001) with age in our subjects, who ranged from the late teens to early 70s. The high upper limit of the frequency of brief arousals was not altered by exclusion of patients who snored or had witnessed apneas or daytime sleepiness. It is important that those scoring arousals on routine polysomnography recognize that high arousal frequencies occur in the normal population on 1-night polysomnography.

Airway resistance increases during sleep. We have determined the ventilatory and arousal responses to the addition of inspiratory resistance of 4, 7, or 10 cmH2O/L/s during sleep in 10 normal men who slept wearing valved face masks. Insufficient ventilatory response data were obtained during rapid eye movement (REM) sleep to allow adequate analysis. The immediate responses to loading were decreases in tidal volume (VT), breathing frequency (f), and minute ventilation (VE), with no difference between wakefulness and Stage 2 and Stage 3/4 sleep in the effects of loading on VT and VE, but f fell more during wakefulness than during sleep (p less than 0.05) because of a greater lengthening of inspired time (TI) (p less than 0.05). During the first 10 breaths, occlusion pressure (P0.1) increased similarly in all EEG stages. Averaging responses during the 2-min periods when resistances were applied, the only variable to differ between EEG stages was TI, which increased more in wakefulness than in Stage 2 or Stage 3/4 sleep (p less than 0.01). Arousal within 2 min of application of resistance occurred less frequently from Stage 3/4 sleep than from Stage 2 or REM sleep (p less than 0.02). The study demonstrates that sleep modifies the changes in respiratory timing produced by resistive loading without having a major effect on ventilation or P0.1 responses. The low frequency of arousal from Stage 3/4 sleep with loading may explain why asthmatics rarely awaken from this stage with wheeze.