Mechanical Properties, Anatomy, and Control of the Upper Airway

2021 ◽  
pp. 27-64
Author(s):  
Denise Dewald ◽  
Kingman P. Strohl
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Neuromuscular Control ◽  
Sleep Health ◽  
Genioglossus Muscle ◽  
Obstructive Sleep ◽  
Wall Stiffness ◽  
Maxilla And Mandible ◽  
And Control

The physiology of the upper airway is fundamental to current and trending therapy for obstructive sleep apnea and neurostimulation in particular. Proper functioning of the upper airway will promote sleep health by supporting the requisite airflow without snoring or significant flow limitation. Dysfunction produces snoring, obstructive hypopneas, and the metabolic sequelae of sleep disordered breathing. How a particular section of the upper airway (e.g., velopharynx, oropharynx, or hypopharynx) remains open while it is suspended from the skull base, maxilla, and mandible is the result of anatomy and neuromuscular control. The genioglossus muscle, originally designed for bringing food into the mouth and swallowing, along with multiple other muscles, participates in the maintenance of patency of the muscular pharynx during wakefulness and sleep. If the genioglossus were the only muscle important for airway stability, then hypoglossal nerve stimulation would likely be universally rather than selectively effective; instead, its effectiveness is predicted by velopharyngeal functions, which in terms of sleep health are poorly described. Literature clearly indicates a fundamental role for muscles other than the genioglossus in maintaining airway diameter, shape, and wall stiffness. Models that incorporate a more complete neuromechanical coupling of these components are necessary to understand a stable airway during sleep and helpful for decisions in management of obstructive sleep apnea.

scholarly journals Cervical Sympathetic Neurofibroma Masquerading as Obstructive Sleep Apnea Syndrome

2011 ◽  
Vol 1 (2) ◽  
pp. 84-87
Author(s):  
M Gopinath ◽  
VV Ramachandran ◽  
Rohini Jose
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Apnea Syndrome ◽  
Upper Airway ◽  
Neuromuscular Control ◽  
Transcervical Approach ◽  
Airway Collapse ◽  
Upper Airway Collapse ◽  
Obstructive Sleep ◽  
Cervical Sympathetic

ABSTRACT Obstructive sleep apnea is a chronic condition characterized by frequent episodes of upper airway collapse during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway, neuromuscular control, or both, which play key roles in the pathogenesis of obstructive sleep apnea. Neurofibromas of the parapharyngeal space are the second most commonly encountered primary tumor of the nerve sheath origin. A parapharyngeal neurofibroma of the cervical sympathetic chain, presenting as obstructive sleep apnea with all the features mimicking that condition is reported here for its rarity in modern clinical practice. A transcervical approach was adopted to excise the tumor in toto, following which patient was completely relieved of the symptoms, especially those of respiratory distress and features of OSAS.

scholarly journals The The relationship between NLRP3 rs10159239 and Vaspin rs2236242 gene variants and obstructive sleep apnea

2021 ◽  
Vol 126 (1) ◽  
Author(s):  
Buğra Kerget ◽  
Ferhan Kerget ◽  
Çiğdem Yüce Kahraman ◽  
Alperen Aksakal ◽  
Ömer Araz
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Control Group ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Obstructive Sleep ◽  
And Control ◽  
The Relationship ◽  
Increased Susceptibility

Background: In obstructive sleep apnea (OSA), recurrent upper airway obstruction and apnea/hypopnea episodes result in endothelial dysfunction, which leads to the release of many proinflammatory cytokines and reactive oxygen species (ROS). ROS induces NLRP3, a protein involved in the synthesis of interleukin (IL)-1 and IL-18; vaspin is a serine protease inhibitor that has an important role in suppressing the activation of NLRP3 inflammasome. In this study, we aimed to investigate the effect of NLRP3 rs10159239 (rs9239) and vaspin rs2236242 (rs6242) single nucleotide polymorphisms (SNPs) on OSA development. Methods: This study included 220 individuals who underwent polysomnography (118 patients with OSA and 102 healthy controls). NLRP3 rs9239 and vaspin rs6242 mutation frequencies were analyzed. Results: The NLRP3 rs9239 SNP genotype analysis revealed no statistically significant differences between the OSA and control groups. In the vaspin gene analysis, the rs6242 AA genotype was significantly more frequent in the OSA group compared with the control group, while the AT genotype was more frequent in controls (P = 0.004, P = 0.02). Comparison of rs6242 allele levels showed that the A allele was significantly more frequent in OSA patients than in controls (P = 0.03). The AA genotype was significantly more frequent in patients with severe OSA than in patients with mild or moderate OSA and the control group (P = 0.001 for all). Serum vaspin levels were significantly lower in carriers of the AA genotype than those with AT and TT genotypes (P = 0.001). Conclusion: The vaspin rs6242 SNP AA genotype increased susceptibility to OSA, while the AT genotype appeared to be protective. The lower plasma vaspin levels in OSA compared with the control group and in patients with the AA genotype suggest that vaspin may be a protective biomarker for OSA.

scholarly journals Modelling mucosal surface roughness in the human velopharynx: a computational fluid dynamics study of healthy and obstructive sleep apnea airways

2018 ◽  
Vol 125 (6) ◽  
pp. 1821-1831
Author(s):  
Christopher Lambeth ◽  
Ziyu Wang ◽  
Kristina Kairaitis ◽  
Abouzar Moshfegh ◽  
Ahmad Jabbarzadeh ◽  
...  
Keyword(s):  
Surface Roughness ◽  
Obstructive Sleep Apnea ◽  
Shear Stress ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Fold Increase ◽  
Mucosal Surface ◽  
Airway Collapse ◽  
Obstructive Sleep ◽  
And Control

We previously published a unique methodology for quantifying human velopharyngeal mucosal surface topography and found increased mucosal surface roughness in patients with obstructive sleep apnea (OSA). In fluid mechanics, surface roughness is associated with increased frictional pressure losses and resistance. This study used computational fluid dynamics (CFD) to analyze the mechanistic effect of different levels of mucosal surface roughness on velopharyngeal airflow. Reconstructed velopharyngeal models from OSA and control subjects were modified, giving each model three levels of roughness, quantified by the curvature-based surface roughness index (CBSRI0.6) (range 24.8–68.6 mm−1). CFD using the k-ω shear stress transport turbulence model was performed (unidirectional, inspiratory, steady-state, 15l/min volumetric flow rate), and the effects of roughness on flow velocity, intraluminal pressure, wall shear stress, and velopharyngeal resistance ( Rv) were examined. Across all models, increasing roughness increased maximum flow velocity, wall shear stress, and flow disruption while decreasing intraluminal pressures. Linear mixed effects modeling demonstrated a log-linear relationship between CBSRI0.6 and Rv, with a common slope (log( Rv)/CBSRI0.6) of 0.0079 [95% confidence interval (CI) 0.0015–0.0143; P = 0.019] for all subjects, equating to a 1.9-fold increase in Rv when roughness increased from control to OSA levels. At any fixed CBSRI0.6, the estimated difference in log( Rv) between OSA and control models was 0.9382 (95% CI 0.0032–1.8732; P = 0.049), equating to an 8.7-fold increase in Rv. This study supports the hypothesis that increasing mucosal surface roughness increases velopharyngeal airway resistance, particularly for anatomically narrower OSA airways, and may thus contribute to increased vulnerability to upper airway collapse in patients with OSA. NEW & NOTEWORTHY Increased mucosal surface roughness in the velopharynx of patients with obstructive sleep apnea (OSA) has recently been identified, but its role in OSA pathogenesis is unknown. This is the first study to model the impact of increased roughness on airflow mechanics in the velopharynx. We report that increasing roughness significantly affects airflow, increasing velopharyngeal resistance and potentially increasing the vulnerability to upper airway collapse, particularly in those patients with an already compromised anatomy.

scholarly journals Upper airway neuromuscular compensation during sleep is defective in obstructive sleep apnea

2008 ◽  
Vol 105 (1) ◽  
pp. 197-205 ◽  
Author(s):  
Brian M. McGinley ◽  
Alan R. Schwartz ◽  
Hartmut Schneider ◽  
Jason P. Kirkness ◽  
Philip L. Smith ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Obstruction ◽  
Upper Airway ◽  
Neuromuscular Control ◽  
Upper Airway Obstruction ◽  
Transient Conditions ◽  
Obstructive Sleep ◽  
Neuromuscular Responses ◽  
Nasal Pressure

Obstructive sleep apnea is the result of repeated episodes of upper airway obstruction during sleep. Recent evidence indicates that alterations in upper airway anatomy and disturbances in neuromuscular control both play a role in the pathogenesis of obstructive sleep apnea. We hypothesized that subjects without sleep apnea are more capable of mounting vigorous neuromuscular responses to upper airway obstruction than subjects with sleep apnea. To address this hypothesis we lowered nasal pressure to induce upper airway obstruction to the verge of periodic obstructive hypopneas (cycling threshold). Ten patients with obstructive sleep apnea and nine weight-, age-, and sex-matched controls were studied during sleep. Responses in genioglossal electromyography (EMGGG) activity (tonic, peak phasic, and phasic EMGGG), maximal inspiratory airflow (VImax), and pharyngeal transmural pressure (PTM) were assessed during similar degrees of sustained conditions of upper airway obstruction and compared with those obtained at a similar nasal pressure under transient conditions. Control compared with sleep apnea subjects demonstrated greater EMGGG, VImax, and PTM responses at comparable levels of mechanical and ventilatory stimuli at the cycling threshold, during sustained compared with transient periods of upper airway obstruction. Furthermore, the increases in EMGGG activity in control compared with sleep apnea subjects were observed in the tonic but not the phasic component of the EMG response. We conclude that sustained periods of upper airway obstruction induce greater increases in tonic EMGGG, VImax, and PTM in control subjects. Our findings suggest that neuromuscular responses protect individuals without sleep apnea from developing upper airway obstruction during sleep.

scholarly journals Obesity and upper airway control during sleep

2010 ◽  
Vol 108 (2) ◽  
pp. 430-435 ◽  
Author(s):  
Alan R. Schwartz ◽  
Susheel P. Patil ◽  
Samuel Squier ◽  
Hartmut Schneider ◽  
Jason P. Kirkness ◽  
...  
Keyword(s):  
Weight Loss ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Neuromuscular Control ◽  
Current Evidence ◽  
Central Adiposity ◽  
Neural Responses ◽  
Humoral Factors ◽  
Obstructive Sleep

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.

scholarly journals Anatomical Balance of the Upper Airway and Obstructive Sleep Apnea

2008 ◽  
Vol 108 (6) ◽  
pp. 1009-1015 ◽  
Author(s):  
Satoru Tsuiki ◽  
Shiroh Isono ◽  
Teruhiko Ishikawa ◽  
Yoshihiro Yamashiro ◽  
Koichiro Tatsumi ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Adult Male ◽  
Upper Airway ◽  
Cross Sectional ◽  
Pharyngeal Airway ◽  
Soft Tissue Volume ◽  
Obstructive Sleep ◽  
Lateral Cephalograms ◽  
Maxilla And Mandible

Background Obesity and craniofacial abnormalities such as small maxilla and mandible are common features of patients with obstructive sleep apnea (OSA). The authors hypothesized that anatomical imbalance between the upper airway soft-tissue volume and the craniofacial size (rather than each alone) may result in pharyngeal airway obstruction during sleep, and therefore development of OSA. Methods Blind measurements of tongue cross-sectional area and craniofacial dimensions were performed through lateral cephalograms in 50 adult male patients with OSA and 55 adult male non-OSA subjects with various craniofacial dimensions. Results Maxillomandibular dimensions were matched between OSA and non-OSA groups. While the tongue was significantly larger in subjects with larger maxillomandible dimensions, OSA patients had a significantly larger tongue for a given maxillomandible size than non-OSA subjects. The hypothesis was also supported in subgroups matched for both body mass index and maxillomandible dimensions. Conclusions Upper airway anatomical imbalance is involved in the pathogenesis of OSA.

Aerodynamics Analysis of the Impact of Nasal Surgery on Patients with Obstructive Sleep Apnea and Nasal Obstruction

ORL ◽  
2021 ◽  
pp. 1-8
Author(s):  
Lifeng Li ◽  
Demin Han ◽  
Hongrui Zang ◽  
Nyall R. London
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Nasal Obstruction ◽  
Upper Airway ◽  
Apnea Hypopnea Index ◽  
Nasal Surgery ◽  
Subjective Sleep Quality ◽  
Obstructive Sleep ◽  
Significant Difference ◽  
The Impact

<b><i>Objective:</i></b> The purpose of this study was to evaluate the effects of nasal surgery on airflow characteristics in patients with obstructive sleep apnea (OSA) by comparing the alterations of airflow characteristics within the nasal and palatopharyngeal cavities. <b><i>Methods:</i></b> Thirty patients with OSA and nasal obstruction who underwent nasal surgery were enrolled. A pre- and postoperative 3-dimensional model was constructed, and alterations of airflow characteristics were assessed using the method of computational fluid dynamics. The other subjective and objective clinical indices were also assessed. <b><i>Results:</i></b> By comparison with the preoperative value, all postoperative subjective symptoms statistically improved (<i>p</i> &#x3c; 0.05), while the Apnea-Hypopnea Index (AHI) changed little (<i>p</i> = 0.492); the postoperative airflow velocity and pressure in both nasal and palatopharyngeal cavities, nasal and palatopharyngeal pressure differences, and total upper airway resistance statistically decreased (all <i>p</i> &#x3c; 0.01). A significant difference was derived for correlation between the alteration of simulation metrics with subjective improvements (<i>p</i> &#x3c; 0.05), except with the AHI (<i>p</i> &#x3e; 0.05). <b><i>Conclusion:</i></b> Nasal surgery can decrease the total resistance of the upper airway and increase the nasal airflow volume and subjective sleep quality in patients with OSA and nasal obstruction. The altered airflow characteristics might contribute to the postoperative reduction of pharyngeal collapse in a subset of OSA patients.

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