scholarly journals Reply to: Weight Loss and Upper Airway Anatomy in Patients with Obstructive Sleep Apnea

Author(s):  
Richard J Schwab ◽  
Brendan T Keenan ◽  
David B. Sarwer ◽  
Allan I Pack
1988 ◽  
Vol 138 (5) ◽  
pp. 1192-1195 ◽  
Author(s):  
I. Rubinstein ◽  
N. Colapinto ◽  
L. E. Rotstein ◽  
I. G. Brown ◽  
V. Hoffstein

2016 ◽  
Vol 21 ◽  
pp. 19-27 ◽  
Author(s):  
Hui Chen ◽  
Ghizlane Aarab ◽  
Maurits H.T. de Ruiter ◽  
Jan de Lange ◽  
Frank Lobbezoo ◽  
...  

2014 ◽  
Vol 116 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Jerome A. Dempsey ◽  
Ailiang Xie ◽  
David S. Patz ◽  
David Wang

We review evidence in support of significant contributions to the pathogenesis of obstructive sleep apnea (OSA) from pathophysiological factors beyond the well-accepted importance of airway anatomy. Emphasis is placed on contributions from neurochemical control of central respiratory motor output through its effects on output stability, upper airway dilator muscle activation, and arousability. In turn, we consider the evidence demonstrating effective treatment of OSA via approaches that address each of these pathophysiologic risk factors. Finally, a case is made for combining treatments aimed at both anatomical and ventilatory control system deficiencies and for individualizing treatment to address a patient 's own specific risk factors.


1991 ◽  
Vol 144 (3_pt_1) ◽  
pp. 494-498 ◽  
Author(s):  
Alan R. Schwartz ◽  
Avram R. Gold ◽  
Norman Schubert ◽  
Alexandra Stryzak ◽  
Robert A. Wise ◽  
...  

2010 ◽  
Vol 108 (2) ◽  
pp. 430-435 ◽  
Author(s):  
Alan R. Schwartz ◽  
Susheel P. Patil ◽  
Samuel Squier ◽  
Hartmut Schneider ◽  
Jason P. Kirkness ◽  
...  

Mechanisms linking obesity with upper airway dysfunction in obstructive sleep apnea are reviewed. Obstructive sleep apnea is due to alterations in upper airway anatomy and neuromuscular control. Upper airway structural alterations in obesity are related to adipose deposition around the pharynx, which can increase its collapsibility or critical pressure (Pcrit). In addition, obesity and, particularly, central adiposity lead to reductions in resting lung volume, resulting in loss of caudal traction on upper airway structures and parallel increases in pharyngeal collapsibility. Metabolic and humoral factors that promote central adiposity may contribute to these alterations in upper airway mechanical function and increase sleep apnea susceptibility. In contrast, neural responses to upper airway obstruction can mitigate these mechanical loads and restore pharyngeal patency during sleep. Current evidence suggests that these responses can improve with weight loss. Improvements in these neural responses with weight loss may be related to a decline in systemic and local pharyngeal concentrations of specific inflammatory mediators with somnogenic effects.


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