Timing of spontaneous sleep‐paralysis episodes
Todd A. Girard, J. Allan Cheyne
Journal of Sleep Research June 1, 2006 DOI: 10.1111/j.1365-2869.2006.00512.x (opens in new tab)
Summary
AI-generated from the abstractSleep paralysis episodes occur most often in the first two hours after going to bed, with just over a quarter happening within the first hour, though episodes can occur throughout the night with a smaller peak near normal waking time. The timing of episodes is consistent for individuals across different nights and does not depend on what time they go to bed. The results support the idea that sleep paralysis timing is controlled by processes that start at or after sleep onset and suggest that sleep paralysis may result from failing to maintain sleep during REM periods at any point in the night, rather than only at sleep onset.
Study at a glance
| Characteristics | Prospective naturalistic field study Peer reviewed |
|---|---|
| Sample size | 348 |
| Population | Regular sleep paralysis experiencers who had previously completed a screening assessment and general sleep survey |
| Key finding | Sleep paralysis episodes are most frequent in the first two hours after bedtime, with a minor mode near normal waking time, and latencies are moderately consistent across episodes and independent of bedtimes. |
Abstract
SummaryThe objective of this prospective naturalistic field study was to determine the distribution of naturally occurring sleep‐paralysis (SP) episodes over the course of nocturnal sleep and their relation to bedtimes. Regular SP experiencers (N = 348) who had previously filled out a screening assessment for SP as well as a general sleep survey were recruited. Participants reported, online over the World Wide Web, using a standard reporting form, bedtimes and subsequent latencies of spontaneous episodes of SP occurring in their homes shortly after their occurrence. The distribution of SP episodes over nights was skewed to the first 2 h following bedtime. Just over one quarter of SP episodes occurred within 1 h of bedtime, although episodes were reported throughout the night with a minor mode around the time of normal waking. SP latencies following bedtimes were moderately consistent across episodes and independent of bedtimes. Additionally, profiles of SP latencies validated self‐reported hypnagogic, hypnomesic, and hypnopompic SP categories, as occurring near the beginning, middle, and end of the night/sleep period respectively. Results are consistent with the hypothesis that SP timing is controlled by mechanisms initiated at or following sleep onset. These results also suggest that SP, rather than uniquely reflecting anomalous sleep‐onset rapid eye movement (REM) periods, may result from failure to maintain sleep during REM periods at any point during the sleep period. On this view, SP may sometimes reflect the maintenance of REM consciousness when waking and SP hallucinations the continuation of dream experiences into waking life.