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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 272-273, (2003)
© 2003 American Thoracic Society

Pro/Con Editorial

Rebuttal from Dr. Schwab

Dr. Strohl argues that sleep apnea is not an anatomical disease because "the closure of the pharyngeal airway occurs during sleep." I agree with him that upper airway muscle tone is decreased during sleep and is an important component of obstructive sleep apnea. The key point, however, which is missing from his presentation, is that this reduction in muscle tone is only important if there is underlying abnormal upper airway anatomy. Subjects with normal upper airway anatomy do not develop obstructive sleep apnea during sleep. If sleep apnea is only a "neurologic" disorder, then everyone should develop sleep disordered breathing when they fall asleep. This is obviously not the case. Several studies have demonstrated a reduction in the caliber of the upper airway in normal subjects during sleep (presumably secondary to a reduction in the activity of upper airway dilator muscles), although these subjects do not develop sleep apnea (1, 2). Thus, state-dependent reductions in upper airway caliber are not by themselves a sine qua non for the development of obstructive sleep apnea. Moreover, why would weight loss, continuous positive airway pressure, oral appliances, or upper airway surgery effectively treat sleep apnea if sleep-disordered breathing is only related to neurophysiologic changes in sleep? These treatment options have not been conclusively shown to increase upper airway muscle tone, although they have been shown to increase upper airway caliber in normal subjects and patients with sleep apnea (3–5).

Dr. Strohl's primary argument is that a reduction in muscle tone or decreased EMG activity leads to the initiation of apnea. Although this assumption is likely correct, there are few data demonstrating a coupling between the mechanical performance of the upper airway muscles and a reduction in EMG activity of these muscles. Studies have not definitively shown that decreased EMG activity of a particular muscle is directly associated with a decrease in upper airway caliber. Such studies are necessary to prove the assertion that a reduction in EMG activity produces a decrease in the caliber of the upper airway. Once such studies are performed, however, I believe Dr. Strohl will find that only subjects with abnormal upper airway anatomy will develop upper airway closure with a reduction in neuromuscular drive during sleep. Subjects with normal upper airway anatomy do not develop sleep apnea, even though there is a reduction in the activity of their upper airway dilator muscles during sleep.

REFERENCES

  1. Schwab RJ, Gupta KB, Gefter WB, Hoffman EA, Pack AI. Upper airway soft tissue anatomy in normals and patients with sleep disordered breathing: significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152:1673–1689.[Abstract]
  2. Rowley JA, Sanders CS, Zahn BR, Badr MS. Effect of REM sleep on retroglossal cross-sectional area and compliance in normal subjects. J Appl Physiol 2001;91:239–248.[Abstract/Free Full Text]
  3. Welch KC, Foster GD, Ritter CT, Schellenberg JB, Wadden TA, Arens R, Maislin G, Schwab RJ. A novel volumetric magnetic resonance imaging paradigm to study upper airway anatomy. Sleep 2002;25:532–542.[Medline]
  4. Sher AE. Upper airway surgery for obstructive sleep apnea. Sleep Med Rev 2002;6:195–212.[CrossRef][Medline]
  5. Schwab RJ, Pack AI, Gupta KB, Metzger LJ, Oh E, Getsy JE, Hoffman EA, Gefter WB. Upper airway and soft tissue structural changes induced by CPAP in normal subjects. Am J Respir Crit Care Med 1996;154:1106–1116.[Abstract]



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Copyright © 2003 American Thoracic Society