© 2003 American Thoracic Society
The Upper Airway and Sleep-disordered BreathingGetting the Big PictureDivision of Pulmonary, Allergy & Critical Care Medicine University of Pittsburgh Sleep Medicine Center Montefiore University Hospital Pittsburgh, Pennsylvania It has long been recognized that for what on casual consideration may appear to be a simple tube, the upper airway is deceptively and enigmatically complex. The nature of its function and dysfunction in the pathogenesis of obstructive sleep apnea–hypopnea has been the focus of research for 3 decades. Physiologic studies examining the properties of this structure have revealed accentuated collapsibility during sleep in patients with obstructive sleep apnea–hypopnea relative to normal subjects and individuals who snore but do not exhibit apneas or hypopneas (1). Although not surprising, given that, by definition, patients with sleep apnea–hypopnea experience upper airway obstruction during sleep, this research provided quantifiable evidence of functional impairment characterizing the upper airway. To further define the operational nature of the abnormality by examining the interplay between the upper airway walls and intraluminal physics, subsequent studies assessed the timing of closure with reference to the breathing cycle (2, 3). The data demonstrated panphasic dysfunction, with collapse during expiration, suggesting inherent abnormality of the pharyngeal wall over and above any inadequate inspiratory activation of the dilator muscles. These issues notwithstanding, the upper airway may be perceived as an anatomic piece of real estate in which location, location, location, with respect to structural and/or functional abnormality, is physiologically and therapeutically important. Efforts to identify a particular site(s) of obstruction by measuring pressure–flow relationships at various upper airway levels revealed that obstruction often, but not always, occurs at the retropalatal level (4). Although providing important information, these studies focused on the hole rather than the doughnut (5). They could not therefore yield definitive insights regarding the interaction(s) among various upper airway structures or the specifically abnormal feature(s) of the pharyngeal wall, which confer susceptibility to collapse during sleep in patients with apneas and hypopneas. It was recognized early on that imaging is well suited to accomplish this task. During the 1980s, investigations using lateral upper airway fluoroscopy and video endoscopy confirmed the findings of physiologic studies and highlighted the complexity of upper airway dysfunction in patients by demonstrating that the level of obstruction varies within and across patients, involving both primary and secondary sites of occlusion (6–9). A composite picture of the luminal configuration and pharyngeal wall soft tissue constituents awaited application of computerized tomography and magnetic resonance imaging with comparative assessments of patients and normal subjects. Early reports using these techniques were limited to analyses of data obtained from axial views. Subsequently, sagittal views were also acquired, adding perspectives on luminal configuration and facilitating volumetric analyses. Although several studies have demonstrated increased parapharyngeal adiposity in patients with obstructive sleep apnea–hypopnea (5, 10, 11), the investigators at the University of Pennsylvania have provided compelling evidence that lateral pharyngeal wall thickening is singularly associated with upper airway narrowing during sleep (12) and that patients with sleep apnea–hypopnea have abnormally thick lateral pharyngeal walls that encroach on the pharyngeal lumen, even during wakefulness (5). In the current issue of AJRCCM (pp. 522–530), Schwab and coworkers (13) used three-dimensional volumetric magnetic resonance imaging of the upper airway during wakefulness in a case–control study of individuals with and without obstructive sleep apnea–hypopnea. The investigators quantified and compared distinct anatomic soft tissue structures across the two groups and calculated the odds ratio for obstructive sleep apnea–hypopnea conferred by increased volume of each. In light of their earlier observations (5, 12), it is not surprising that the data support the investigators' primary hypothesis that upper airway soft tissue volume is increased in this disorder. The volumes of the retropalatal and retroglossal lateral pharyngeal walls, soft palate, tongue, and genioglossus muscle were significantly greater in patients with obstructive sleep apnea–hypopnea, even after adjustment for covariates including parapharyngeal fat (as a reflection of neck visceral fat), gender, ethnicity, and craniofacial configuration. Accordingly, it is intuitively appealing that even after adjusting for visceral adipose tissue in the neck, the likelihood of obstructive sleep apnea–hypopnea was enhanced by larger volumes of almost all soft tissue structures, with particular risk conferred by increased lateral pharyngeal wall and tongue volume. A very tangible bonus of the imaging technique used by Schwab and coworkers (13) is represented by the narrated video that accompanies the article. This provides an opportunity to visualize the upper airway and the soft tissues that embrace it, in rotating color-coded three dimensions. It is evident that the configuration of a given upper airway segment is influenced by the function of the longitudinally adjacent regions. It is unlikely that such images, striking as they may be, will replace numerically descriptive data that permit statistical analyses. However, visualizing the upper airway and surrounding structures in multidimensional perspectives provides synergistic conceptual understanding of form and function over and above that conveyed by means and standard deviations. More than just illustrating anatomic detail, three-dimensional volumetric video imaging of the upper airway structures may prove to be a useful tool in understanding how factors that are external to the airway translate into obstructive sleep apnea–hypopnea. For example, this technique may provide unique insights regarding the mechanism(s) through which different hormonal exposures impact soft tissue elements and adversely influence upper airway stability during sleep (14, 15). Similarly, as Schwab and coworkers (13) comment, the imaging methodology used in their study may be an excellent tool to explore how genetic factors operationalize to increased risk for apneas and hypopneas. In future, we might expect these investigators as well as others to extend volumetric assessments by using faster image acquisition techniques to even more dynamically examine the upper airway and its behavior during sleep in normal individuals and patients. Information obtained in this fashion may also have an immediate impact on the clinical care of patients by identifying the offending upper airway segments with subsequent therapeutic targeting. Schwab and coworkers have taken us one more step toward getting the big picture of obstructive sleep apnea–hypopnea. Acknowledgments M.H.S. is a scientific consultant to Respironics, Inc. and a coinventor of BiPAP(r) with a financial interest in this device brand. REFERENCES
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