Citation

Martin SE, Brander PE, Deary IJ, Douglas NJ. J. Sleep Res. 1999; 8(4): 305-311.

Affiliation

Department of Medicine, University of Edinburgh, Royal Infirmary, UK.

Copyright

(Copyright © 1999, European Sleep Research Society, Publisher John Wiley and Sons)

DOI

unavailable

PMID

10646171

Abstract

Previously, we found that regular sleep fragmentation, similar to that found in patients with sleep apnoea/hypopnoea syndrome (SAHS), impairs daytime function. Apnoeas and hypopnoeas occur in groups in patients with REM or posture related SAHS. Thus, we hypothesised that clustered sleep fragmentation would have a similar impact on daytime function as regular sleep fragmentation. We studied 16 subjects over two pairs of 2 nights and 2 days. The first night of each pair was for acclimatisation. On the second night, subjects either had their sleep fragmented regularly every 90 s, or fragmented every 30 s for 30 min every 90 min, the remaining 60 min being undisturbed. We fragmented sleep with tones to produce a minimum 3 s increase in EEG frequency. During the days following each pair of nights we tested subjects daytime function. Total sleep time (TST) and microarousal frequency were similar no both study nights. We found significantly less stage 2 (55 SD 4, 62 +/- 7%; P = 0.001) and more slow wave sleep (21 SD 3, 12 +/- 6%; P < 0.001) on the clustered night. Mean sleep onset latency was similar on MSLT (clustered 10 SD 5, regular 9 +/- 4 min; P = 0.7) and MWT (clustered 32 SD 7, regular 30 +/- 7 min; P = 0.2). There was no difference in subjects mood or cognitive function after either study night. These results suggest that although there is more slow wave sleep (SWS) on the clustered night, similar numbers of sleep fragmenting events produced similar daytime function whether the events were evenly spaced or clustered.

Language: en