ORP rises to wake levels during arousals and then decreases as sleep resumes. The return to deep sleep occurs in two phases, a fast phase that is complete within 9-seconds after the end of arousal, followed by a slow component (Figure). ORP-9 is the average ORP over the 9 seconds after the end of the arousal (1). If ORP-9 is high, further reduction occurs at a slow rate, and the brain remains in a highly arousable state following arousal, with the result that event/arousal recurrence is more likely to occur following a previous event, resetting ORP up. This results in suspension of ORP at a high level (shallow sleep) or, at best, very slow progression to deep sleep. A High ORP-9 indicates that high arousability is much more likely to be the result of abnormal central regulation of sleep depth. In patients with unstable upper airway and high ORP-9, arousal is likely to occur soon after the sleep-induced obstruction and interrupt the recruitment of pharyngeal dilators, leading to recurrence of events. Conversely, subjects in whom sleep becomes quite deep immediately after arousal (low ORP-9) can tolerate the obstruction for a longer time, allowing the reflex recruitment of dilator muscles, thereby increasing the probability of resolving the obstruction without arousal (2). Existing data (1), and unpublished analysis of the SHHS data (3) confirm the existence of highly significant correlations between ORP-9 and AHI and ORP-9 and the arousal awakening index, but effect sizes were small (0.02 and 0.01, respectively, for the SHHS data).

 

ORP-9 varies over a wide range in people with no OSA or insomnia (1.15 (0.80–1.56); (3)) but can be as high as 2.00 in some patients with OSA. Relative to this wide interindividual range, ORP-9 changes little (≈0.1) in response to acute or long-term (3-4 weeks) correction of the OSA with CPAP (4,5), suggesting that high ORP-9 promotes high AHI and arousals and not the other way around. It was proposed that a higher frequency of arousals (e.g., with high AHI) results in earlier termination of the slow phase of sleep depth recovery, accounting for the higher ORPNR ((1); arrows in panel C of the figure below). ORP-9 decreases little (≈0.15) following 36-hour total sleep deprivation (unpublished observation from reference 6), suggesting that it is also not very sensitive to sleep pressure. These observations and the fact that it is quite reproducible when remeasured after 5 years ((3); panel D in the figure below) suggest that it is a trait.

 

The average and range of ORP-9 in patients with insomnia and normal wake time are very similar to the average and range in subjects with neither insomnia nor OSA (7). By contrast, in half the patients with insomnia and excessive wake time, ORP-9 was completely above the range found in patients with normal wake time (>1.50). This suggests that slow recovery after arousals (high ORP-9) plays an important role in many (but not all) patients with objective insomnia. Whether those with high ORP-9 respond differently to insomnia therapy remains to be determined.

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Accordingly, the main use of ORP-9 is to determine whether central slowing of sleep depth recovery (high ORP-9) is contributing to excessive sleep fragmentation and/or excessive wake time.