Clinical reviewPeripheral neuropathology of the upper airway in obstructive sleep apnea syndrome
Introduction
Obstructive sleep apnea syndrome (OSAS) is a common, chronic disorder that is characterized by sleep fragmentation due to apnea, hypopnea, and repeated arousals resulting from partial or complete closure of the upper airway, and occurs in patients of all ages. An essential component in the pathogenesis of OSAS is an increase in upper airway resistance and obstruction that may result from either upper airway anatomical abnormalities or problems related to neuromuscular control of the upper airway.
Though the precise contributions of neuromuscular and anatomical factors on OSA pathogenesis are still debated,1, 2, 3 it is clear that there is a significant role for neuromuscular response in keeping the upper airway patent.
Section snippets
Pathogenesis of OSAS
The human upper airway serves as a multipurpose structure for tasks of speech and deglutition, and as an air passage for breathing. Though the upper airway is composed of numerous muscles and soft tissues, it lacks a rigid support, particularly between the hard palate and the larynx. This lack of bony or cartilaginous support facilitates finely tuned phonation and articulation, but also makes the upper airway vulnerable to collapse, especially during physiological changes in sleep. In addition
Afferent sensory receptors
There are different types of sensory receptors in the upper airway. These receptors respond to pressure, respiratory muscle drive, cold, heat, irritants, and other chemicals. Among these receptors, the mechanoreceptors of the upper airway have been well studied.
The mechanoreceptors of the upper airway respond to changes in airway pressure, airflow, temperature, and to upper airway muscle tone.19 Though there is no direct evidence that these receptors are affected in OSAS, there is indirect
Possible causes of UA neuropathy in OSAS: vibration, desaturation or inflammation?
The exact cause of neuropathy in OSAS patients is not fully understood. Most OSAS patients snore due to vibration of upper airway soft tissues resulting from a narrow or partially occluded upper airway.46 Persistent vibratory trauma resulting in nerve impairment affecting the hands and arms of workers, have been well documented.47 This occurs due to prolonged exposure to vibrating tools. Therefore, it is possible that the same type of vibratory trauma may be induced in the upper airway due to
Morphological (histological) assessment: light & electron microscope
The sub-occlusive stage of habitual snoring usually precedes the development of OSAS, but the pathophysiological mechanisms underlying this progression are not known. Histological changes indicative of a denervation process of the efferent pathways to the palatopharyngeus muscle was demonstrated in OSAS patients42 and has been explained above. Furthermore, focal degeneration of myelinated nerve fibers was shown in the uvula of severe OSAS patients, and an afferent nerve lesion with impaired
Conclusion
Apart from anatomical narrowing of the upper airway as a pathogenetic mechanism in the development of OSAS, there is mounting evidence to suggest the role of neuropathy in the upper airway as well.77, *98, 99 Both the vibration caused by snoring and the hypoxia caused by intermittent upper airway collapse may affect nerves in the upper airway. These changes can impair the normal function of the upper airway mucosa (sensory) and the pharyngeal dilator muscles (motor), rendering the upper airway
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Interoception relates to sleep and sleep disorders
2020, Current Opinion in Behavioral SciencesCitation Excerpt :The disbalance toward negative experiences may have long-standing consequences, as recent studies have found that the affective signatures of negative emotional experiences could persist through extinction learning, across the night, and over the long term in people with ID [60–63]. With respect to sleep disorders other than ID, accumulating evidence suggests that OSA is associated with impaired mechano- and thermosensitivity of the upper airway resulting from local neuropathy [64,65]. A recent study systematically examined the functional integrity of afferent neural pathways from the palate by means of electrical stimulation with alternating currents at different frequencies and found in patients with OSA impaired perception specifically of large fiber-mediated afferents at the soft palate [66].
Mandibular advancement reveals long-term suppression of breathing discomfort in patients with obstructive sleep apnea syndrome
2019, Respiratory Physiology and NeurobiologyCitation Excerpt :In OSAS patients, several types of neural lesions could interfere with this process and explained both blunted perception of inspiratory resistive loading (Tun et al., 2000) and our present results. These lesions include peripheral pharyngeal neuropathy (Sunnergren et al., 2011; Tsai et al., 2013) that could blunt the perception of respiratory abnormalities in the same way as it blunts the perception of mucosal airflow (Dematteis et al., 2005) or the perception of cold (Sunnergren et al., 2011). Central nervous system lesions could also interfere with the central processing of respiratory stimuli.
Serotnin as a possible biomarker in obstructive sleep apnea
2016, Sleep Medicine ReviewsCitation Excerpt :LAMP can be detected directly through measuring the change of refractive index in the bulk LAMP solution with SPR sensing methods [104]. Several biomarkers have emerged as providing important information regarding respiratory status and specifically the presence of OSA [105]. 5-HT in particular may be harnessed as a specific biomarker for OSA diagnostic testing.
The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation
2013, Free Radical Biology and MedicineDenervation-Associated Change in the Palatinus and Levator Veli Palatini Muscles of Dogs with Elongated Soft Palate
2016, Journal of Comparative PathologyCitation Excerpt :The muscle lesions in the soft palate observed in BAOS, like those in OSAS, may also be caused by physical stress. Some studies have described peripheral nerve degeneration as a cause of myofibre group atrophy and myofibre type grouping in the soft palate and uvula of people with OSAS, and have speculated that physical stress may induce peripheral neuropathy, which results in denervation myopathy (Edström et al., 1992; Friberg et al., 1998; Bassiouny et al., 2009; De Bellis et al., 2012; Tsai et al., 2013). A decrease in the number of peripheral nerve branches has also been demonstrated within the ESPs of dogs with BAOS (Arai et al., 2016).
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The most important references are denoted by an asterisk.