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Arousals from sleep and hypoxia are both thought to contribute to the waking neurobehavioral symptoms of Obstructive Sleep Apnea or OSA. However, there are varied other changes in sleep associated with this syndrome. Among 1,521 patients with OSAS evaluated with polysomnography at the University of Pennslvania Sleep Disorders Center, the number of arousals per hour ranged from 0 to 130, with Respiratory Distress Indices increasing from an average of 4 in the least frequent arousal group (0-15/hr), to 9 in the next most frequent (15-25), 23 in the next (25-50), 52 in the next (50-75) and 89 in those with most frequent arousals (75-130). Correspondingly, total sleep time decreased from 331 minutes to 322 to 298 to 275 to 233, and stage 1 sleep increased from 43 to 50 to 60 to 67 to 61 minutes, therefore representing an increasing proportion of total sleep time (from 13% to 26%), with corresponding decreases in slow wave and REM sleep, increased "sleep fragmentation" and loss of sleep continuity as arousals increased in frequency. Invoking the concept of "sleep consolidation," one researcher observed that mild sleep apneics have relatively long periods of 20-90 minutes of consolidated sleep between bursts of apnea, while severe sleep apneics (AHI greater than 45) never slept as long as 10 minutes without an apneic event.
Sleep fragmentation has been induced experimentally, such as by sounds, in healthy individuals with the same relationships between frequency of arousals and changes in sleep patterns. As frequency of sleep fragmentation increases in these people, the restorative effects of sleep are lost, MSLT sleep latencies decrease, and mood and performance both suffer.
There are various types of "arousals," the least frequent being actual awakenings, especially in OSA patients, whereas increases in muscle tone as measured by the EMG are most frequent, although other kinds of arousal may involve movement, shifts from one stage of sleep to another, increased frequence of brain waves, and appearance of alpha waves. In healthy subjects, full or partial awakenings cause the greatest sleep disturbance and waking deficits.
In sleep apneics, four levels of arousals ranged from an increase in EEG frequency and chin EMG (level), to shorter (2A) or longer (2B) alpha bursts, to stage shifts to lighter sleep (3) to partial (4A) or full (4B) awakenings. Compared to healthy controls, patients with periodic leg movements, and insomniacs, OSA patients had more level 1 and 2 arousals but not more level 4 arousals (ie, not more awakenings). The combination of level 1 and 2 arousals best predicted sleepiness defined by the MSLT.
Healthy people become more difficult to awaken as sleep fragmentation accumulates, which may explain why sleep apneics don't show a high frequency of awakenings and often aren't aware of having disturbed sleep. That is, the chronic disruption of sleep continuity may lead to increasing pressure to sleep. Sleep fragmentation also increases amnesia for arousals and awakenings, and lead to increased sleep inertia--the great difficulty sleep apneics often have getting going in the morning, or after a nap. In other words, the sleep system in sleep apneics is constantly trying to compensate for the sleep loss; any improvement in sleep, especially if it allows consolidated sleep to occur for ten minutes or more, will provide some recuperative benefits, as witnessed by the marked improvement some sleep apneics feel after their first night of CPAP.
The correlation between RDI (AHI) and waking symptoms has always been present but never especially strong, for unclear rasons. Some factors which may confound this relationship include RDI not reliably reflecting EEG arousals, which may be quite subtle; the importance of periods of consolidated sleep may make RDI less meaningful if the events are clustered, allowing for some sleep consolidation, than if they are spread out throughout sleep; individuals who have basically different levels of function aside from effects of OSA may continue to have differences in functioning that mask the correlation of functioning with RDI across individuals. The relationship between RDI and functional impairment holds up well only across a wide range of RDIs and not so well in narrower ranges, so that for example it may be difficult to show that an apneic with an AHI of 30 functions worse than one with an AHI of 15, but easier to show that the apneic with an AHI of 60 has worse functioning. Unfortunately, experimental studies with normal subjects have not closely modelled the sleep fragmentation seen in sleep apneics, both in terms of the frequency of arousals (generally equivalent to AHI well below 20) and the type of arousals (ie, levels 4A and 4B vs. 1 and 2).
This article is more of a review than a report of new research, but it does incorporate a good deal of data and, most importantly, introduces concepts important to the understanding of how sleep apnea may work to cause daytime symptoms of sleepiness, inattentiveness, forgetfulness, and mood swings. These are probably less related to brain hypoxia than to fragmentation of sleep by "arousals" which do not represent full or even partial awakenings. To the extent that such fragmentation--which prevents the consolidation of sleep (at least 10 minutes of continuous deep or slow wave sleep seems important for restorative effects)--lies at the basis of these symptoms, any source of increased sleep fragmentation--be it periodic leg movements of sleep, the sounds and movements of a bed partner, the sleeping environment, the discomfort of wearing a CPAP mask or the sound of the machine, slippage of the headgear or venting of air through the mouth or the sides of the mask, etc, etc--may feed into the same underlying pathological process causing symptoms. Therefore, it may be unrealistic to expect that the simple application of a CPAP pressure judged appropriate in the sleep lab will resolve all symptoms of sleep fragmentation, if there are other factors operating to fragment sleep in the home environment.
About four years ago, after I had been on CPAP over two years and still experienced excessive daytime drowsiness and frequent napping, I travelled to the West Coast take a one-week course in sleep medicine which I was very worried I wouldn't be able to stay awake well enough to attend fully. I surprised myself pleasantly by being able to limit myself to a single one-hour nap which I took in place of lunch, and feeling considerably more refreshed than usual each morning. I sensed that my commitment to the course was helping to limit my napping and consolidate better my nighttime sleep, but I also noticed relief from not being awakened by my favorite bed partners: my two dogs, one of whom seemed to have a lot of nighttime restlessness himself! Nevertheless, it took me three years after that to finally decide the dogs were indeed a source of sleep fragmentation for me, and to exile them from the bedroom, all of us I imagine a bit broken-hearted, but my own sleep considerably less disturbed!
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