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.

Improvement in Upper Airway Function after Weight Loss in Patients with Obstructive Sleep Apnea

1988 ◽  
Vol 138 (5) ◽  
pp. 1192-1195 ◽  
Author(s):  
I. Rubinstein ◽  
N. Colapinto ◽  
L. E. Rotstein ◽  
I. G. Brown ◽  
V. Hoffstein
Keyword(s):  
Weight Loss ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Airway Function ◽  
Obstructive Sleep

scholarly journals Obstructive Sleep Apnea in Neurodegenerative Disorders: Current Evidence in Support of Benefit from Sleep Apnea Treatment

2020 ◽  
Vol 9 (2) ◽  
pp. 297 ◽  
Author(s):  
Annie C. Lajoie ◽  
Anne-Louise Lafontaine ◽  
R. John Kimoff ◽  
Marta Kaminska
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Current Knowledge ◽  
Upper Airway ◽  
Current Evidence ◽  
Obstructive Sleep ◽  
Intermittent Hypoxemia ◽  
And Function ◽  
The Impact ◽  
Sleep Apnea Treatment

Obstructive sleep apnea (OSA) is a prevalent disorder characterized by recurrent upper airway obstruction during sleep resulting in intermittent hypoxemia and sleep fragmentation. Research has recently increasingly focused on the impact of OSA on the brain’s structure and function, in particular as this relates to neurodegenerative diseases. This article reviews the links between OSA and neurodegenerative disease, focusing on Parkinson’s disease, including proposed pathogenic mechanisms and current knowledge on the effects of treatment.

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.

Effect of Weight Loss on Upper Airway Collapsibility in Obstructive Sleep Apnea

1991 ◽  
Vol 144 (3_pt_1) ◽  
pp. 494-498 ◽  
Author(s):  
Alan R. Schwartz ◽  
Avram R. Gold ◽  
Norman Schubert ◽  
Alexandra Stryzak ◽  
Robert A. Wise ◽  
...  
Keyword(s):  
Weight Loss ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

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 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.

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