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Functional role of neural injury in obstructive sleep apnea.

Saboisky JP, Butler JE, Gandevia SC, Eckert DJ - Front Neurol (2012)

Bottom Line: Multiple studies have demonstrated altered sensory and motor function in patients with OSA using a variety of neurophysiological and histological approaches.However, the extent to which the alterations contribute to impairments in upper airway muscle function, and thus OSA disease progression, remains uncertain.Some unresolved questions including possible treatment targets are noted.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Australia Sydney, NSW, Australia.

ABSTRACT
The causes of obstructive sleep apnea (OSA) are multifactorial. Neural injury affecting the upper airway muscles due to repetitive exposure to intermittent hypoxia and/or mechanical strain resulting from snoring and recurrent upper airway closure have been proposed to contribute to OSA disease progression. Multiple studies have demonstrated altered sensory and motor function in patients with OSA using a variety of neurophysiological and histological approaches. However, the extent to which the alterations contribute to impairments in upper airway muscle function, and thus OSA disease progression, remains uncertain. This brief review, primarily focused on data in humans, summarizes: (1) the evidence for upper airway sensorimotor injury in OSA and (2) current understanding of how these changes affect upper airway function and their potential to change OSA progression. Some unresolved questions including possible treatment targets are noted.

No MeSH data available.


Related in: MedlinePlus

Types of evidence for neuromuscular pathology in OSA. MUSCLE: Remodelling may be reflected via anatomical changes within the upper airway muscles (red); EFFERENT: changes in the electromyogram (EMG) of the upper airway muscles innervated via the cranial nerves (blue); AFFERENT: changes in sensory pathways (green). NCAM=neural cell adhesion molecule.
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Figure 1: Types of evidence for neuromuscular pathology in OSA. MUSCLE: Remodelling may be reflected via anatomical changes within the upper airway muscles (red); EFFERENT: changes in the electromyogram (EMG) of the upper airway muscles innervated via the cranial nerves (blue); AFFERENT: changes in sensory pathways (green). NCAM=neural cell adhesion molecule.

Mentions: The extent to which snoring and hypoxia exacerbate the disease and lead to important damage is unresolved. In this review, some of the more convincing evidence for and against upper airway remodeling in which data have been acquired in both OSA patients and non-OSA controls is highlighted. We review the pathophysiological evidence under three separate headings: (1) anatomical remodeling of the upper airway muscles, (2) efferent changes, and (3) afferent changes (see Figure 1). This encompasses evidence from a variety of neurophysiological approaches including histological, electrophysiological, and physiological studies. The function of upper airway reflexes and tongue force/fatigue characteristics in OSA vs. non-OSA subjects is also briefly reviewed. Finally, we discuss how upper airway remodeling and neural injury might contribute to upper airway closure during sleep.


Functional role of neural injury in obstructive sleep apnea.

Saboisky JP, Butler JE, Gandevia SC, Eckert DJ - Front Neurol (2012)

Types of evidence for neuromuscular pathology in OSA. MUSCLE: Remodelling may be reflected via anatomical changes within the upper airway muscles (red); EFFERENT: changes in the electromyogram (EMG) of the upper airway muscles innervated via the cranial nerves (blue); AFFERENT: changes in sensory pathways (green). NCAM=neural cell adhesion molecule.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3375463&req=5

Figure 1: Types of evidence for neuromuscular pathology in OSA. MUSCLE: Remodelling may be reflected via anatomical changes within the upper airway muscles (red); EFFERENT: changes in the electromyogram (EMG) of the upper airway muscles innervated via the cranial nerves (blue); AFFERENT: changes in sensory pathways (green). NCAM=neural cell adhesion molecule.
Mentions: The extent to which snoring and hypoxia exacerbate the disease and lead to important damage is unresolved. In this review, some of the more convincing evidence for and against upper airway remodeling in which data have been acquired in both OSA patients and non-OSA controls is highlighted. We review the pathophysiological evidence under three separate headings: (1) anatomical remodeling of the upper airway muscles, (2) efferent changes, and (3) afferent changes (see Figure 1). This encompasses evidence from a variety of neurophysiological approaches including histological, electrophysiological, and physiological studies. The function of upper airway reflexes and tongue force/fatigue characteristics in OSA vs. non-OSA subjects is also briefly reviewed. Finally, we discuss how upper airway remodeling and neural injury might contribute to upper airway closure during sleep.

Bottom Line: Multiple studies have demonstrated altered sensory and motor function in patients with OSA using a variety of neurophysiological and histological approaches.However, the extent to which the alterations contribute to impairments in upper airway muscle function, and thus OSA disease progression, remains uncertain.Some unresolved questions including possible treatment targets are noted.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Australia Sydney, NSW, Australia.

ABSTRACT
The causes of obstructive sleep apnea (OSA) are multifactorial. Neural injury affecting the upper airway muscles due to repetitive exposure to intermittent hypoxia and/or mechanical strain resulting from snoring and recurrent upper airway closure have been proposed to contribute to OSA disease progression. Multiple studies have demonstrated altered sensory and motor function in patients with OSA using a variety of neurophysiological and histological approaches. However, the extent to which the alterations contribute to impairments in upper airway muscle function, and thus OSA disease progression, remains uncertain. This brief review, primarily focused on data in humans, summarizes: (1) the evidence for upper airway sensorimotor injury in OSA and (2) current understanding of how these changes affect upper airway function and their potential to change OSA progression. Some unresolved questions including possible treatment targets are noted.

No MeSH data available.


Related in: MedlinePlus