ABSTRACT
INTRODUCTION The most accepted theory regarding the pathogenesis of obstructive sleep apnea (OSA) centers on an anatomical deficiency in the upper airway. During sleep, the loss of neuromuscular compensatory mechanisms present during wakefulness is combined with the abnormal upper airway anatomy to favor upper airway collapse. Some of the earliest reports of OSA have recognized that recurrent upper airway (UA) collapse during sleep is the key pathogenic factor (1,2). Early treatment consisted of bypassing the UA by tracheostomy and subsequent work by Remmers et al. localized the pharynx as the site of UA collapse (3). Despite much progress in the field, the reasons behind the recurrent collapse of the UA and the timing of UA collapse during sleep remains to be clearly defined.
