The human upper airway and its neuromechanical behaviour


Obstructive sleep apnoea is a common disorder which is linked to increased incidence of stroke, myocardial infarction and heart failure (for review see Jordan et al 2014).  However, the fundamental neuromotor control of the upper airway is poorly understood, perhaps because of its structural and neural complexity.  Recently a series of reviews tackled critical central and peripheral issues in its control (Journal of Applied Physiology, February 2014, volume 116).  Here is a summary of our approach.

 

The upper airway wall is shown in black, soft tissue in red, and bony structures in gray. A: In research the upper airway is usually modeled as a collapsible tube. B: The dashed black line indicates reduced pharyngeal area as tissue mass increases in the confined space in the back of the mouth. C: Bony structures bound the oral cavity, so that compression of the tongue in one location requires expansion elsewhere. If there is spare space within the oral cavity, the tongue expands without encroaching on the airway (left), but, if space is limited due to a larger soft tissue volume, then this will result in encroachment on the airway.

The upper airway wall is shown in black, soft tissue in red, and bony structures in gray. A: In research the upper airway is usually modeled as a collapsible tube. B: The dashed black line indicates reduced pharyngeal area as tissue mass increases in the confined space in the back of the mouth. C: Bony structures bound the oral cavity, so that compression of the tongue in one location requires expansion elsewhere. If there is spare space within the oral cavity, the tongue expands without encroaching on the airway (left), but, if space is limited due to a larger soft tissue volume, then this will result in encroachment on the airway.

Magnetic resonance elastography, an MRI-based technique, relies on the principle that the propagation of a vibration wave through tissue depends on its mechanical properties. In upper airway elastography, a vibration from a mouth guard propagates through bones into the tongue and soft palate. The top panel identifies the key anatomical structures and the two lower panels show the elastic properties for a normal subject and a matched obstructive sleep apnea (OSA) patient. Note the lower stiffness in the tongue of the OSA patient. Dashed lines outline the tongue and soft palate.

Magnetic resonance elastography, an MRI-based technique, relies on the principle that the propagation of a vibration wave through tissue depends on its mechanical properties. In upper airway elastography, a vibration from a mouth guard propagates through bones into the tongue and soft palate. The top panel identifies the key anatomical structures and the two lower panels show the elastic properties for a normal subject and a matched obstructive sleep apnea (OSA) patient. Note the lower stiffness in the tongue of the OSA patient. Dashed lines outline the tongue and soft palate.

WHAT DID WE FIND?

The upper airway is a complicated, multifunctional, dynamic neuromechanical system: it is critically involved in breathing, swallowing and speech.  Its patency during breathing requires moment-to-moment coordination of neural and mechanical behaviour and this must vary with posture of the head and neck.  Failure to continuously recruit and coordinate the airway dilator muscles to counterbalance the forces that act to shut the airway results in hypopneas or apneas.  Repeated failures lead to obstructive sleep apnea (OSA).  Obesity and anatomical variations, such as retrognathia, increase the likelihood of upper airway collapse by altering the passive mechanical behaviour of the upper airway.  This behaviour depends on the mechanical properties of each upper airway tissue in isolation, their geometrical arrangements, and their physiological interactions.  Our new measurements of respiratory-related movement and deformation of the airway wall and its muscles (such as genioglossus) using tagged magnetic resonance imaging have shown that there are different patterns of airway soft tissue movement during the respiratory cycle (e.g. Cheng et al 2008).  Furthermore, in OSA patients, we find that airway dilation appears poorly coordinated compared with that in healthy subjects matched for body mass index and movement is minimal in those with very severe OSA (Brown et al 2013).  Intrinsic mechanical properties of airway tissues are altered in OSA patients, but the factors underlying these changes have yet to be elucidated.  It is likely that both central and peripheral factors influence upper airway collapsibility differently in different patients (e.g. Eckert et al 2013).  How neural drive to the airway dilator muscles such as genioglossus relates to the biomechanical behaviour of the upper airway (its movement and stiffness) is still unresolved.  Recent studies have shown that the biomechanical behaviour of the upper airway cannot be simply predicted from electromyographic activity (EMG) of its muscles.  So under some circumstances, increased neural drive, expressed as increased EMG, can paradoxically fail to lead to adequate airway dilation.

 

SIGNIFICANCE AND IMPLICATIONS

While this work highlights the special elements of neuromotor control that must apply to the upper airway, at the same time, the novel technical and other approaches used to study it should have application for understanding different motor systems such as those involved in limb and trunk movement.

 

PUBLICATION

 

Bilston L & Gandevia S (2014). Biomechanical properties of the human upper airway and their effect on its behavior during breathing and in obstructive sleep apneaJ Appl Physiol 116, 314 –324.

 

KEY REFERENCES

Brown EC, Cheng S, McKenzie DK, Butler JE, Gandevia SC, Bilston LE (2013). Respiratory movement of upper airway tissue in obstructive sleep apnea. Sleep 36, 1069-76.
Cheng S, Butler JE, Gandevia SC, Bilston LE (2008). Movement of the tongue during normal breathing in awake healthy humans. J Physiol 586, 4283-94
Eckert DJ, White DP, Jordan AS, Malhotra A, Wellman A (2013). Defining phenotypic causes of obstructive sleep apnea. Identification of novel therapeutic targets. Am J Respir Crit Care Med 188, 996-1004
Jordan AS, McSharry DG, Malhotra A (2014). Adult obstructive sleep apnoea. Lancet 383, 736-47.

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