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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
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.2
3
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.
In traditional sleep staging, visual inspection of the EEG is used to determine the presence or absence of SWS and to determine the proportion of the scoring epoch during which SWS is present. Continuous quantification of cortical SWA during sleep, as performed by the authors, can be achieved through computerized spectral analysis. For this analysis, the digitized EEG is subjected to a fast Fourier transformation to determine the frequency composition of the waveform. SWA in this study was defined as the sum of the power (in microvolts squared) between 0.75 and 4.5 cps. As spectral analysis is valid only for stationary waveforms, short segments of the EEG (4-s epochs, in this study) are analyzed in sequence to approximate a stationary wave.
To better understand the study, the reader should be aware of several factors in the design: (1) as detailed above, SWS and SWA are related but not the same; in addition, the method of measuring SWA is not standard or necessarily easily applied in clinical practice; (2) the MSLT is only one measure of daytime sleepiness and may not correlate highly with other outcomes, such as neuropsychological tests,4 quality of life,5 simulated driving tests,6 and subjective feelings of sleepiness7 8 9 ; (3) the MSLT as used by the authors is not standard but is a modification of the recommended experimental MSLT; specifically, the 20-s epochs are not recommended, and the definition of sleep onset and the use of 10 min of sleep are not standard10 ; and (4) the study number is small, with 7 to 10 subjects with SAS and 10 control subjects being analyzed.
How the design features affect the conclusions or application of the results is speculative, but the reader should be cautious in attempting to apply the results to current clinical practice.
To confirm the current observations, a larger study should be done using not only the MSLT but also other measures of daytime sleepiness and function such as the Epworth Sleepiness Scale,7 11 the maintenance of wakefulness test,8 and quality-of-life measures.12 In addition, the concept that SWA (but not SWS) during the first NREM period is critical in daytime function needs to be confirmed in different settings. For example, if the hypothesis is correct, then treatment of SAS to reduce daytime sleepiness may only require treatment of the first 2 h of sleep with minimal benefit of longer treatment. In general, it may be possible to sleep for 2 h and not suffer most of the consequences of sleep deprivation. If this concept can be applied not only to the SAS but to other conditions, this may have major implications for shift workers, soldiers, and others.
If the observations of this study are confirmed, sleep medicine practitioners may need to revise the current standard scoring system for staging NREM sleep. Speculatively, SWA may be staged as a substitute for SWS using criteria of 0.75 to 4.5 cps with no amplitude requirements. This may require modifying the approach to handling sleep recordings since it may be difficult to score SWA by visual inspection. Instead, spectral analysis may become the preferred approach. In addition, scoring of the first NREM-rapid-eye-movement (REM) cycle for SWA may provide predictive value for the degree of daytime sleepiness. Improvement in SWA of the first NREM-REM cycle with treatment in SAS may provide predictive value for successful management of daytime sleepiness. In addition, this study provides a greater rationale for staging sleep, even in patients with obvious obstructive sleep apnea.
It is also possible that the observations of this study may not be applicable to clinical sleep staging. Instead, the observations may help design further research to understand sleep factors that influence daytime function. Ultimately, this research may help design better diagnostic and treatment strategies for patients with daytime sleepiness from various sleep disorders.
References
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