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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 108, (2003)
© 2003 American Thoracic Society


Pro/Con Editorial

Rebuttal from Dr. Pollak

What is Black's argument? First, that EDS may persist despite "what would appear to be adequate treatment" of OSA. Second, that this residual EDS is "not uncommon." Third, that it should be treated with the wake-promoting drug, modafinil.

Let us consider each point in turn. First, does residual EDS really exist? The one study cited by Black as evidence of residual EDS (1) was flawed by the absence of an objective measure of CPAP compliance. When compliance was measured, in a study that also gave evidence of residual EDS (2), it was termed "disappointing." Yet, even suboptimal treatments yield dramatic improvement of MSLT scores. EDS can indeed be eliminated by CPAP (e.g., Reference 3)—strong evidence that EDS is caused by OSA.

Black next claims that cases of residual EDS are "not uncommon." In the next breath, he admits that their prevalence is unknown. If it were true that residual EDS is not uncommon, the causative link between OSA and EDS would be called into question. It is much more likely, however, that OSA does cause EDS, as we have seen, making "residual EDS" a consequence of inadequately treated OSA.

It is possible, of course, that residual EDS does exist as an independent disorder, one that is not caused by OSA but only brought out by it. In that case, we would be dealing with a new disorder of wakefulness that shares pathogenesis with that of OSA. The resulting violation of Occam's razor is not worthwhile, however, because we remain a long way from proving the existence of such a disorder.

Black next cites preliminary evidence that modafinil reduces EDS, whether OSA has been treated or not. His point is irrelevant. No one claims that modafinil is ineffective, and even Black would probably not claim that its effect is specific.

It is good that people like Black are working on the problem of "residual EDS" but, until they come up with evidence that residual EDS exists as a distinct disorder of wakefulness, clinicians should continue to assume that EDS associated with OSA is caused by OSA. It should therefore fully respond to CPAP, implying that modafinil at present has no role in the management of sleep apnea.

REFERENCES

  1. Morisson F, Decary A, Petit D, Lavigne G, Malo J, Montplaisir J. Daytime sleepiness and EEG spectral analysis in apneic patients before and after treatment with continuous positive airway pressure. Chest 2001;119:45–52.[Abstract/Free Full Text]
  2. Engleman HM, Cheshire KE, Deary IJ, Douglas NJ. Daytime sleepiness, cognitive performance and mood after continuous positive airway pressure for the sleep apnoea/hypopnoea syndrome. Thorax 1993;48: 911–914.[Abstract]
  3. Jenkinson C, Davies RJ, Mullins R, Stradling JR. Comparison of therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised prospective parallel trial. Lancet 1999;353:2100–2105.[CrossRef][Medline]



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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2003 American Thoracic Society