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For at least 25 years, patients who have undergone sleep polysomnography or PSG have complained that the constraints of the PSG leads and other equipment make them sleep supine--on their backs--more than they normally would at home, but no research was done to confirm this until now. The authors considered it important because patients with positional obstructive sleep apnea or positional OSA (see Glossary) would have more respiratory events while lying on their backs than on their sides, and therefore more events overall during PSG than at home when free to lie on their sides. This might lead to an overestimation of the apnea-hypopnea index (AHI) (see Glossary) in the lab compared to the unrestricted home environment. Twelve patients, 11 men and 1 woman, ages 24 to 74, with mild to moderate OSA (AHI=11-51) seen at Mr. Sinai, diagnosed with positional OSA on the basis of AHI while lying on their backs twice or more as great as that recorded on their sides, were included. They all had laboratory PSGs done and scored routinely except that their definitions of apnea and hypopnea required a drop in oxygen saturation (see Glossary) of 4% or greater, to allow for comparison with nights with subsequent nights of recording without the full PSG apparatus attached. Subjects, who were told only that they were investigating the effect of PSG on sleep, not the effect of sleep position, were to return for two more nights in the lab during which only pulse oximetry (see Glossary) was recorded, and taped videorecording allowed for two raters to asess sleep position as either supine, on the right side, or on the left side. Oxygen desaturations were used to compare frequency of apneas/hypopneas on the initial PSG night compared to the two non-PSG nights. Most (9/12) subjects spent considerably less sleeping time on their backs during the non-PSG compared to the PSG nights, the group as a whole averaging about 3 1/4 hours on their backs on the PSG nights and about 2 hrs on their backs during the non-PSG nights, out of an average of 7 hours in bed on all nights. The difference in sleep position between PSG and non-PSG nights was statistically significant, but there was no significant difference in the desaturation index between the nights, with only a non-significant trend towards self-reported better sleep during non-PSG nights. The authors also noted that during the PSG night only one subject spent any time in the prone (lying on the stomach) position versus 4-6 subjects during the non-PSG nights, but this was no otherwise studied. They consider that their confirmation of the PSG effect on amount of sleep time spent in the supine position might have clinical implications for patients with marginal sleep apnea, possibly referred for evaluation for snoring alone without other symptoms, who might meet diagnostic criteria only because of being forced to sleep more in the supine position than they would ordinarily. They doubted this would apply to patients with severe OSA. They also suggested that an overestimation of the severity of OSA due to this position effect might lead to neglect of other factors--such as periodic leg movements of sleep or narcolepsy--that might also be present and contributing to hypersomnia, a relatively common occurrence. The authors suggested that their failure to detect a difference in desaturation index between PSG and non-PSG nights might have resulted from (a) the mildness of the sleep apnea not allowing a sufficient range of possible decrease; (b) the use of desaturation index instead of true AHI may have reduced sensitivity to true obstructive events; and (c) they used the time in bed, rather than the time asleep, to calculate the desaturation index, probably further reducing its sensitivity since actual sleep time may have been greater during non-PSG than PSG nights. They noted in passing the marked inhibition of prone sleep time on PSG versus non-PSG nights, but considered this less important as the prone position was not known to affect severity of OSA.

Few people who have undergone polysomnography will be surprised by these findings. Through about a dozen sleep studies over the past six years, I have always been conscious of the tendency to pull on the electrodes when I move about at night. I do have positional sleep apnea, and as far as I know I spend most of my time at home sleeping on my side rather than my back. But it seems not only uncomfortable, but inconvenient to the technicians who have to come in to replace electrodes, and disturbing to me for them to do so, if I move from side to side and pull them off. I have also been conscious of other effects on my normal sleep patterns of sleeping in the lab. If I was at home and awakened during the night, I would often get up and get something to eat, that seemed to relax me, but felt unable to do this in the lab. If I were having a lot of trouble sleeping on a given night, I would become quite conscious that a technician was observing this and possibly having difficulty getting an adequate sleep recording--which awareness made sleep even more difficult. The lab generally allowed me to go to sleep when I wished, but I knew they would awaken me the next morning about 6 a.m., whereas often I might sleep much later. Of course, I was usually glad to get released as soon as possible! It is hard for me to remember back to the days before I was on CPAP, but it is obvious to me that nowadays I don't sleep on my stomach simply because this is next to impossible wearing a CPAP mask. Admittedly, it could be done by building up a support of pillows and then hanging one's head over the other side, but this would in turn seem likely to make uncomfortable any attempt to sleep in another position, like on one's side. I don't especially miss the prone sleeping position but I don't feel comfortable in dismissing, as the authors do, the possibility that some subjects may sleep much better, with less apneas, in this position, just because it is hard to study them and apply CPAP in this position! Whenever I see a study using an "index" of respiratory distress different from the usual clinical AHI because of practical constraints of the study protocol, I feel uncomfortable with the results--and this happens quite often. Substitution of desaturations for actual respiratory-related arousals seems all the less satisfactory as increasing evidence suggests that mere respiratory effort without even hypopneas (the so called upper airway resistance syndrome) can cause arousals, and that arousals may be more important than oxygen desaturations in causing sleep fragmentation and important symptoms of sleep apnea. Time in bed is obviously not the same as time asleep, and all the less valid whenever one compares two situations where one might expect the patient to sleep better in one than the other. Finally, there is an issue the authors do not even bring up: the question whether CPAP pressures optimized for a typical laboratory night of half-supine, half on-the-side sleep, are the same as they would be in the natural home situation where only perhaps a quarter of the time is spent in the supine position. I myself am not aware of data bearing on positional differences in optimal CPAP pressure, but without such data I wouldn't assume them to be the same. If they were different, this would result in frequent mismatching of laboratory-determined pressures and actual patient pressure needs, with widespread effects of presumably excessive pressures and suboptimal control of sleep apnea in the home environment, contributing the the much-mentioned problem of poor compliance.

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