2023
DOI: 10.1016/j.resp.2023.104033
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Primary site of constriction during the compression phase of cough in healthy young adults

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Cited by 4 publications
(4 citation statements)
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“…Structural changes may limit one's ability to coordinate breathing and swallowing, or generate adequate pressure for high velocity airflows during cough. These may include: (1) altered compliance of the chest wall, (2) weak/spastic inspiratory (e.g., diaphragm, external intercostals) and expiratory (e.g., abdominals, obliques, internal intercostals) muscles, (3) vocal fold and upper airway pathologies ( 6 , 10 , 12 , 18 , 19 ). Disruptions in neural signaling of sensorimotor pathways may also contribute to hypotussia, including dysfunctional signal reception, transmission, processing, and/or output in one, or several neural substrates: (1) pulmonary, tracheobronchial, and laryngeal receptors that receive cough stimuli input ( 10 , 12 , 25 27 ), (2) vagal afferents of the airways that transmit sensory input to the central nervous system, including internal superior (iSLN) and recurrent laryngeal nerves (RLN) [Box A ] ( 10 , 25 , 26 ), (3) central pattern generators (CPG) for swallow, cough, and breathing integrate sensory input to generate a reconfigured respiratory CPG (rRCPG) to execute cough [Box B ] ( 4 , 28 ), and (4) subcortex and cortical structures involved with filtering, perceiving, and processing discriminative and affective characteristics of the sensory stimuli, leading to execution of volitional cough, or suppression/augmentation of reflexive cough ( 4 , 10 , 12 , 13 , 25 27 , 29 ).…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Structural changes may limit one's ability to coordinate breathing and swallowing, or generate adequate pressure for high velocity airflows during cough. These may include: (1) altered compliance of the chest wall, (2) weak/spastic inspiratory (e.g., diaphragm, external intercostals) and expiratory (e.g., abdominals, obliques, internal intercostals) muscles, (3) vocal fold and upper airway pathologies ( 6 , 10 , 12 , 18 , 19 ). Disruptions in neural signaling of sensorimotor pathways may also contribute to hypotussia, including dysfunctional signal reception, transmission, processing, and/or output in one, or several neural substrates: (1) pulmonary, tracheobronchial, and laryngeal receptors that receive cough stimuli input ( 10 , 12 , 25 27 ), (2) vagal afferents of the airways that transmit sensory input to the central nervous system, including internal superior (iSLN) and recurrent laryngeal nerves (RLN) [Box A ] ( 10 , 25 , 26 ), (3) central pattern generators (CPG) for swallow, cough, and breathing integrate sensory input to generate a reconfigured respiratory CPG (rRCPG) to execute cough [Box B ] ( 4 , 28 ), and (4) subcortex and cortical structures involved with filtering, perceiving, and processing discriminative and affective characteristics of the sensory stimuli, leading to execution of volitional cough, or suppression/augmentation of reflexive cough ( 4 , 10 , 12 , 13 , 25 27 , 29 ).…”
Section: Introductionmentioning
confidence: 99%
“…Cough is a vital, life-sustaining behavior essential for pulmonary homeostasis (1)(2)(3)(4). The major function of cough is to generate the high velocity airflows and shearing forces required to expel unwanted material from the airways and allow breathing to occur unobstructed (1,(5)(6)(7). Unfortunately, disordered cough (or dystussia, Table 1) is quite prevalent, especially in the context of dysphagia or swallowing disorders, exacerbating the risk of the deleterious effects which can be associated with uncompensated aspiration (3,5,18,19).…”
Section: Introductionmentioning
confidence: 99%
“…Structural changes may limit one's ability to coordinate breathing and swallowing, or generate adequate pressure for high velocity airflows during cough. These may include: (1) altered compliance of the chest wall, (2) weak/spastic inspiratory (e.g., diaphragm, external intercostals) and expiratory (e.g., abdominals, obliques, internal intercostals) muscles, (3) vocal fold and upper airway pathologies (6,10,12,18,19). Disruptions in neural signaling of sensorimotor pathways may also contribute to hypotussia, including dysfunctional signal reception, transmission, processing, and/or output in one, or several neural substrates: (1) pulmonary, tracheobronchial, and laryngeal receptors that receive cough stimuli input (10, 12, 25-27), (2) vagal afferents of the airways that transmit sensory input to the central nervous system, including internal superior (iSLN) and recurrent laryngeal nerves (RLN) [Box A] (10, 25, 26), (3) central pattern generators (CPG) for swallow, cough, and breathing integrate sensory input to generate a reconfigured respiratory CPG (rRCPG) to execute cough [Box B] (4, 28), and (4) subcortex and cortical structures involved with filtering, perceiving, and processing discriminative and affective characteristics of the sensory stimuli, leading to execution of volitional cough, or suppression/augmentation of reflexive cough (4,10,12,13,(25)(26)(27)29).…”
Section: Domains Of Hypotussic Cough Interventions: Rehabilitative Vs...mentioning
confidence: 99%
“…Cough is a vital, life-sustaining behavior essential for pulmonary homeostasis (1)(2)(3)(4). The major function of cough is to generate the high velocity airflows and shearing forces required to expel unwanted material from the airways and allow breathing to occur unobstructed (1,(5)(6)(7). Unfortunately, disordered cough (or dystussia, Table 1) is quite prevalent, especially in the context of dysphagia or swallowing disorders, exacerbating the risk of the deleterious effects which can be associated with uncompensated aspiration (3,5,18,19).…”
Section: Introductionmentioning
confidence: 99%