Pathophysiology of Obstructive Sleep Apnea

Horner, Richard L.

doi:10.1097/01.hcr.0000336138.71569.a2

Cited by 63 publications

(48 citation statements)

References 71 publications

(96 reference statements)

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“…Reduced upper airway motoneuron activity and hence muscle tone during sleep is an underlying cause of OSA (Horner, 2008). Diminished airway motor tone results in airway narrowing or complete airway obstruction, which leads to hypoventilation and asphyxia.…”

Section: Scientific Importance and Clinical Relevancementioning

confidence: 99%

“…This is biologically important because breathing is acutely sensitive to and regulated by mechanical feedback from both the lungs and upper airways (Hammouda and Wilson, 1932;Kuna, 1986;Kubin et al, 2006). It is also clinically relevant because intermittent modulation of mechanical feedback during obstructive sleep apnea (OSA), a disorder that afflicts 28 million North Americans (Guilleminault and Abad, 2004;Horner, 2008), could have neuroplastic effects on respiratory motor function.…”

Section: Introductionmentioning

confidence: 99%

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Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Tadjalli¹,

Duffin²,

Peever³

2010

J. Neurosci.

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The respiratory control system is not just reflexive, it is smart, it learns, and, in fact, it has a memory. The respiratory system listens to and carefully remembers how previous stimuli affect breathing. Respiratory memory is laid down by adjusting synaptic strength between respiratory neurons. For example, repeated hypoxic bouts trigger a form of respiratory memory that functions to strengthen the ability of respiratory motoneurons to trigger contraction of breathing muscles. This type of respiratory plasticity is known as long-term facilitation (LTF). Although chemical feedback, such as hypoxia, initiates LTF, it is unknown whether natural modulation of mechanical feedback (from vagal inputs) also causes motor plasticity. Here, we used reverse microdialysis, electrophysiology, neuropharmacology, and histology to determine whether episodic modulation of vagally mediated mechanical feedback is able to induce respiratory LTF in anesthetized adult rats. We show that repeated obstructive apneas disrupt vagal feedback and trigger LTF of hypoglossal motoneuron activity and genioglossus muscle tone. This same stimulus does not cause LTF of diaphragm activity. Hypoxic episodes do not cause apnea-induced LTF; instead, LTF is triggered by modulation of vagal feedback. Unlike hypoxia-induced respiratory plasticity, vagusinduced LTF does not require 5-HT 2 receptors but instead relies on activation of ␣1-adrenergic receptors on hypoglossal motoneurons. In summary, we identify a novel form of hypoxia-and 5-HT-independent respiratory motor plasticity that is triggered by physiological modulation of vagal feedback and is mediated by ␣1-adrenergic receptor activation on (or near) hypoglossal motoneurons.

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Section: Scientific Importance and Clinical Relevancementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Tadjalli¹,

Duffin²,

Peever³

2010

J. Neurosci.

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“…This reduced pharyngeal muscle tone in sleep, by leading to a narrower and more collapsible upper airway, also predisposes to airflow limitation (i.e. hypopnoeas and snoring) and obstructive sleep apnoea in susceptible individuals, such as those with already anatomically narrow upper airways (Horner 2008b). Indeed, in such subjects, the absence of pharyngeal muscle tone can be sufficient to produce an upper airway that is closed, or nearly closed, at pressures close to atmospheric (Kuna & Remmers 2000;Smith & Schwartz 2002;Younes 2008).…”

Section: Overview Of the Respiratory Systemmentioning

confidence: 99%

“…In addition to the nucleus ambiguus that contains motoneurons innervating the laryngeal and pharyngeal muscles, the brainstem also includes motoneurons of the hypoglossal and trigeminal motor nuclei that innervate the muscles of the tongue and soft palate (figure 1a), i.e. muscles important to the maintenance of an open upper airway for effective breathing (Horner 1996(Horner , 2008b. Respiratory-related activity is not restricted to neurons of the ventral and dorsal respiratory groups and cranial motoneurons innervating the pharyngeal and laryngeal muscles, however.…”

Section: Overview Of the Respiratory Systemmentioning

confidence: 99%

Emerging principles and neural substrates underlying tonic sleep-state-dependent influences on respiratory motor activity

Horner

2009

Phil. Trans. R. Soc. B

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Respiratory muscles with dual respiratory and non-respiratory functions (e.g. the pharyngeal and intercostal muscles) show greater suppression of activity in sleep than the diaphragm, a muscle almost entirely devoted to respiratory function. This sleep-related suppression of activity is most apparent in the tonic component of motor activity, which has functional implications of a more collapsible upper airspace in the case of pharyngeal muscles, and decreased functional residual capacity in the case of intercostal muscles. A major source of tonic drive to respiratory motoneurons originates from neurons intimately involved in states of brain arousal, i.e. neurons not classically involved in generating respiratory rhythm and pattern per se. The tonic drive to hypoglossal motoneurons, a respiratory motor pool with both respiratory and non-respiratory functions, is mediated principally by noradrenergic and glutamatergic inputs, these constituting the essential components of the wakefulness stimulus. These tonic excitatory drives are opposed by tonic inhibitory glycinergic and g-amino butyric acid (GABA) inputs that constrain the level of respiratory-related motor activity, with the balance determining net motor tone. In sleep, the excitatory inputs are withdrawn and GABA release into the brainstem is increased, thus decreasing respiratory motor tone and predisposing susceptible individuals to hypoventilation and obstructive sleep apnoea.

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“…OSA is characterized by a partial or complete collapse of the upper airway during sleep, resulting in partial or complete cessations of breathing (hypopnea, apnea), leading to the disruption of normal sleep architecture and oxygen desaturation. 3,4 OSA has a serious effect on the growth and development of a child; if untreated, OSA may lead to significant morbidity including vascular and metabolic disorders and neurocognitive dysfunction, ultimately leading to reduced quality of life and increased medical expenses. 5,6 Oral diseases are major public health issues as a result of considerable function impairment, reduced quality of life, and the costly treatment.…”

Section: Introductionmentioning

confidence: 99%

Oral Health Status of Children With High Risk of Sleep-Disordered Breathing

Tamasas¹,

Godfrey²,

Nelson³

et al. 2018

JDSM

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JDSMStudy Objectives: To evaluate caries, gingival and periodontal status, and oral health-related quality of life (OHRQoL) in children with high risk of sleep-disordered breathing (SDB) in comparison to those with low risk of SDB. Methods:This cross-sectional study recruited consecutive children between the ages of 8 to 17 years from a university-based pediatric dental clinic. Caregivers completed the Pediatric Sleep Questionnaire (PSQ) to stratify risk of SDB. Children and their caregivers completed the Child Oral Health Impact Profile (COHIP) to measure OHRQoL. A dental examination blinded to the results of the PSQ and COHIP was conducted. Group characteristics were compared between those with high risk (SDB+) and low risk for SDB (SDB−). Results:One hundred twenty-three children were enrolled (11.5 ± 2.7 years, female = 48%). Forty-nine percent were classified as SDB+. COHIP scores were higher among the SDB+ group (24.5 versus 11.6, P < .001 as reported by caregivers, and 25.9 versus 10.3, P < .001 as reported by children). The incidence of dental caries present on examination was higher (60% versus 20%, P < .001) in the SDB+ group. In addition, the indices of periodontal diseases were higher among the SDB+ group when compared to the SDB− group (periodontal pocket depth was 2.0 ± 1.0 versus 0.0 ± 0.7, P < .0001, and bleeding on probing was 90% versus 20%, P < .001).Conclusions: This study suggests that caregiver reports of SDB symptoms in those seeking pediatric dental care are common. In addition, children in the SDB+ group had poorer OHRQoL, with increased incidence of caries lesion and periodontal disorders when compared to the SDB− group.

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Pathophysiology of Obstructive Sleep Apnea

Cited by 63 publications

References 71 publications

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

Emerging principles and neural substrates underlying tonic sleep-state-dependent influences on respiratory motor activity

Oral Health Status of Children With High Risk of Sleep-Disordered Breathing

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