© 2003 American Thoracic Society
Rebuttal from Dr. StrohlThe argument for obstructive sleep apnea being an anatomic problem is indeed difficult. Closure of the upper airway during sleep happens in most thin, normal adult men and women almost every time they enter rapid eye movement sleep (1). So how firm is the wisdom of a universally abnormal upper airway in clinical presentations of obstructive sleep apnea?Dr. Schwab points to risk factors and current treatment to confer causality to anatomy. This is problematic. How much would we know of the mechanisms for Type 2 diabetes if we only studied those who were obese? As in diabetes, obesity is a major risk factor, but other factors are important. The highest pretest probability for sleep apnea may well be nocturnal angina with a 15- to 25-fold risk (2), similar in magnitude to cigarette smoking with lung cancer. In comparison, family studies indicate obesity and cephalometry to each add one- to seven-fold risk to the appearance of obstructive apnea (2). Linkage to genomic regions for apnea–hypopnea index can be improved when adjusted for obesity and are unlinked from craniofacial traits (3). Pathogenesis revealed by citation of popular treatment is misleading: strychnine in low doses acutely improves obstructive apneas in humans and does not directly act on body mass or upper airway structures (4). Burwell and coworkers (5) reported only that the "Pickwickian" was a new syndrome to describe polycythemia associated with obesity and respiratory failure, as other diseases known to cause erythocytosis were absent; it took years until a tracheostomy revealed the syndrome's secret. What will we be calling obstructive sleep apnea in the future? I argue that is will be fundamentally linked to brain mechanisms. Indeed, one Roman physician had it right when he treated snoring with needles, presumably waking up upper airway patency in an obese and/or inebriated patient (5). There may be a number of pathways by which one could develop sleep apnea syndrome or an apnea–hypopnea index of clinical import (more than 30 per hour), with obesity and craniofacial anatomy being two important amplifiers of apnea length and frequency. The fundamental event, however, is a neural mechanism that can operate every time we go to sleep. REFERENCES
This article has been cited by other articles:
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
