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Editorials |

To Sleep Deeply, Perchance to Wake Refreshed

Michael Littner, MD, FCCP; Ronald S. Szymusiak, PhD
Author and Funding Information

Affiliations: Sepulveda, CA 
 ,  Dr. Littner is a Professor of Medicine at the UCLA School of Medicine. Dr. Szymusiak is an Associate Professor at the UCLA School of Medicine.

Correspondence to: Michael Littner, MD, FCCP, Veterans Affairs Greater Los Angeles Healthcare System, UCLA School of Medicine, 16111 Plummer St, Sepulveda, CA 91343



Chest. 2001;119(6):1633-1634. doi:10.1378/chest.119.6.1633
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The deepest nonrapid-eye-movement (NREM) sleep stages in humans, stages 3 and 4, are also called slow-wave sleep (SWS) and are defined by the appearance of a substantial amount of large amplitude (≥ 75 μV) slow waves in the cortical EEG, with a frequency of 0 to 2 cycles/s (cps).1 In man, SWS is at a maximum towards the beginning of the night and progressively declines across the sleep period. In all mammalian species studied to date, slow waves increase dramatically during sleep following sleep deprivation. Experimental evidence from human and animal studies suggests that slow waves reflect the homeostatic component of NREM.23 The report in this issue of CHEST by Heinzer et al (see page 1807) details an intriguing hypothesis, namely, that daytime sleepiness, as measured by the multiple sleep latency test (MSLT) in the obstructive sleep apnea syndrome (SAS), is the result of a decrease in slow wave activity (SWA), defined as cortical EEG waves of 0.75 to 4.5 cps (compared with the 0 to 2 cps of SWS) during the first NREM period during sleep. The approach uses spectral analysis, which does not involve an amplitude criteria. The authors conclude that SWA, but not SWS, correlates with the MSLT.

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