Relationship Between Upper Airway Sensation And Dilator Muscle Activation During Sleep In Obstructive Sleep Apnea (OSA)

2011 ◽  
Author(s):  
Emilie Gaudette ◽  
Marisol Dominguez-Alvarez ◽  
Isabelle Boutin ◽  
R J. Kimoff
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Activation ◽  
Upper Airway ◽  
Dilator Muscle ◽  
Obstructive Sleep

scholarly journals Physiology in Medicine: Obstructive sleep apnea pathogenesis and treatment—considerations beyond airway anatomy

2014 ◽  
Vol 116 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Jerome A. Dempsey ◽  
Ailiang Xie ◽  
David S. Patz ◽  
David Wang
Keyword(s):  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Activation ◽  
Upper Airway ◽  
Airway Anatomy ◽  
Output Stability ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Treatment Considerations

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.

scholarly journals Obstructive Sleep Apnea: Emerging Treatments Targeting the Genioglossus Muscle

2019 ◽  
Vol 8 (10) ◽  
pp. 1754 ◽  
Author(s):  
Olga Mediano ◽  
Sofia Romero-Peralta ◽  
Pilar Resano ◽  
Irene Cano-Pumarega ◽  
Manuel Sánchez-de-la-Torre ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Tone ◽  
Treatment Strategies ◽  
Upper Airway ◽  
Apnea Hypopnea Index ◽  
Compensatory Response ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Osa Treatment

Obstructive sleep apnea (OSA) is characterized by repetitive episodes of upper airway obstruction caused by a loss of upper airway dilator muscle tone during sleep and an inadequate compensatory response by these muscles in the context of an anatomically compromised airway. The genioglossus (GG) is the main upper airway dilator muscle. Currently, continuous positive airway pressure is the first-line treatment for OSA. Nevertheless, problems related to poor adherence have been described in some groups of patients. In recent years, new OSA treatment strategies have been developed to improve GG function. (A) Hypoglossal nerve electrical stimulation leads to significant improvements in objective (apnea-hypopnea index, or AHI) and subjective measurements of OSA severity, but its invasive nature limits its application. (B) A recently introduced combination of drugs administered orally before bedtime reduces AHI and improves the responsiveness of the GG. (C) Finally, myofunctional therapy also decreases AHI, and it might be considered in combination with other treatments. Our objective is to review these therapies in order to advance current understanding of the prospects for alternative OSA treatments.

scholarly journals Obstructive Sleep Apnea Syndrome

2021 ◽  
pp. 1577-1589
Author(s):  
Suresh Menon
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Apnea Syndrome ◽  
Upper Airway ◽  
Causative Factor ◽  
Treatment Modalities ◽  
Muscle Physiology ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Apnea Syndrome

AbstractObstructive sleep apnea (OSA) is a condition that occurs due to aberrations in the oropharyngeal anatomy and the upper airway dilator muscle physiology with neurocognitive and cardiovascular sequelae. The mandibular-maxillary complex as the causative factor entails the maxillofacial surgeon to diagnose and treat the case when present, using the different treatment modalities available in the armamentarium.

Asynchrony of lingual muscle recruitment during sleep in obstructive sleep apnea

2015 ◽  
Vol 118 (12) ◽  
pp. 1516-1524 ◽  
Author(s):  
Yaniv Dotan ◽  
Giora Pillar ◽  
Alan R. Schwartz ◽  
Arie Oliven
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Emg Activity ◽  
Muscle Coordination ◽  
Flow Limitation ◽  
Tongue Muscle ◽  
Dilator Muscle ◽  
Obstructive Sleep

Pharyngeal collapsibility during sleep increases primarily due to decline in dilator muscle activity. However, genioglossus EMG is known to increase during apneas and hypopneas, usually without reversing upper airway obstruction or inspiratory flow limitation. The present study was undertaken to test the hypothesis that intense activation of the genioglossus fails to prevent pharyngeal obstruction during sleep, and to evaluate if sleep-induced changes in tongue muscle coordination may be responsible for this phenomenon. We compared genioglossus and tongue retractors EMG activity in 13 obstructive sleep apnea (OSA) patients during wakefulness, while breathing through inspiratory resistors, to the activity observed at the end of apneas and hypopneas after 25 mg of brotizolam, before arousal, at equal esophageal pressure. During wakefulness, resistive breathing triggered increases in both genioglossus and retractor EMG. Activation of agonist tongue muscles differed considerably from that of the arm, as both genioglossus and retractors were activated similarly during all tongue movements. During sleep, flow limitation triggered increases in genioglossal EMG that could reach more than twofold the level observed while awake. In contrast, EMGs of the retractors reached less than half the wakefulness level. In sleeping OSA patients, genioglossal activity may increase during obstructed breathing to levels that exceed substantially those required to prevent pharyngeal collapse during wakefulness. In contrast, coactivation of retractors is deficient during sleep. These findings suggest that sleep-induced alteration in tongue muscle coordination may be responsible for the failure of high genioglossal EMG activity to alleviate flow limitation.

scholarly journals Alteration in upper airway dilator muscle coactivation during sleep: comparison of patients with obstructive sleep apnea and healthy subjects

2018 ◽  
Vol 124 (2) ◽  
pp. 421-429 ◽  
Author(s):  
Ron Oliven ◽  
Guy Cohen ◽  
Yaniv Dotan ◽  
Mostafa Somri ◽  
Alan R. Schwartz ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Healthy Subjects ◽  
Upper Airway ◽  
Retractor Muscle ◽  
Emg Activity ◽  
Muscle Coordination ◽  
Flow Limitation ◽  
Dilator Muscle ◽  
Obstructive Sleep

In patients with obstructive sleep apnea (OSA), substantial increases in genioglossus (GG) activity during hypopneas/apneas usually fail to restore normal airflow. We have previously suggested that sleep-induced alteration in tongue muscle coordination may explain this finding, as retractor muscle coactivation was reduced during sleep compared with wakefulness. The present study was undertaken to evaluate whether these alterations in dilator muscle activation during sleep play a role in the pathogenesis of OSA and whether coactivation of additional peripharyngeal muscles (non-GG muscles: styloglossus, geniohyoid, sternohyoid, and sternocleidomastoid) is also impaired during sleep. We compared GG and non-GG muscle electromyographic (EMG) activity in 8 patients with OSA and 12 healthy subjects during wakefulness while breathing through inspiratory resistors with the activity observed during sleep toward the end of flow limitation, before arousal, at equivalent esophageal pressures. During wakefulness, resistive breathing triggered increases in both GG and non-GG muscle activity. During sleep, flow limitation was associated with increases in GG-EMG that reached, on average, >2-fold the level observed while awake. In contrast, EMGs of the non-GG muscles, recorded simultaneously, reached, on average, only ~2/3 the wakefulness level. We conclude that during sleep GG activity may increase to levels that substantially exceed those sufficient to prevent pharyngeal collapse during wakefulness, whereas other peripharyngeal muscles do not coactivate during sleep in both patients with OSA and healthy subjects. We speculate that upper airway muscle dyssynchrony during sleep may explain why GG-EMG activation fails to alleviate flow limitation and stabilize airway patency during sleep. NEW & NOTEWORTHY Pharyngeal obstruction during sleep may trigger genioglossus activity to levels substantially exceeding those observed during wakefulness, without ameliorating flow limitation. In contrast, other peripharyngeal muscles exhibit a much lower activity during sleep in both patients with obstructive sleep apnea and healthy subjects. Coordinated muscular synergy stabilizes the pharynx despite relatively low activity while awake, yet even higher genioglossal activity allows the pharynx to obstruct when simultaneous activity of other dilator muscles is inadequate during sleep.

Neuromechanical interaction in human snoring and upper airway obstruction

1999 ◽  
Vol 86 (6) ◽  
pp. 1759-1763 ◽  
Author(s):  
Lixi Huang ◽  
John E. Ffowcs Williams
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Negative Pressure ◽  
Muscle Activation ◽  
Fluid Pressure ◽  
Upper Airway ◽  
Obstructive Apnea ◽  
Obstructive Sleep ◽  
Clinical Consequences ◽  
Neuromuscular Functioning

The fact that snoring and obstructive apnea only occur during sleep means that effective neuromuscular functioning of the upper airway during sleep is vital for the maintenance of unimpeded breathing. Recent clinical studies in humans have obtained evidence demonstrating that upper airway neural receptors sense the negative pressure generated by inspiration and “trigger,” with a certain delay, reflex muscle activation to sustain the airway that might otherwise collapse. These findings have enabled us to propose a model in which the mechanics is coupled to the neuromuscular physiology through the generation of reflex wall stiffening proportional to the retarded fluid pressure. Preliminary results on this model exhibit three kinds of behavior typical of unimpeded breathing, snoring, and obstructive sleep apnea, respectively. We suggest that the increased latency of the reflex muscle activation in sleep, together with the reduced strength of the reflex, have important clinical consequences.

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