Physiological and Pathophysiological Implications of Upper Airway Reflexes in Humans.

Nishino, Takashi

doi:10.2170/jjphysiol.50.3

Cited by 106 publications

(65 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast to the paroxysmal and variable degree of closure noted with VCD, laryngospasm refers to sustained intense, virtually complete closure of the vocal folds following direct laryngeal stimulation by irritants [43]. The triggers for laryngospasm are not dissimilar from those for VCD and it may very well be that laryngospasm represents the most severe pathophysiological consequences of the glottic closure reflex.…”

Section: Differential Diagnosismentioning

confidence: 99%

Vocal cord dysfunction: what do we know?

Kenn

Balkissoon²

2010

Eur Respir J

145

View full text Add to dashboard Cite

Vocal cord dysfunction (VCD) is a disorder caused by episodic unintentional paradoxical adduction of the vocal cords, which may induce acute severe dyspnoea attacks not responsive to conventional asthma therapy. The aetiology of VCD is complex and often multifactorial. The essential pathophysiology is that of a hyperfunctional laryngeal reflex to protect the lower airway as a result of any combination of post-nasal drip, gastro-oesophageal reflux, laryngopharyngeal reflux and/or psychological conditions. Laryngoscopic demonstration of the paradoxical motion while wheezing or stridorous is considered the diagnostic gold standard. Speech therapy, including the use of special relaxed-throat breathing patterns is effective for VCD that is purely of the functional nature. Knowledge of the clinical features of VCD and identifying factors that may be contributing to the development of VCD can provide adequate clues to the correct diagnosis and management.

show abstract

Section: Differential Diagnosismentioning

confidence: 99%

Vocal cord dysfunction: what do we know?

Kenn

Balkissoon²

2010

Eur Respir J

145

View full text Add to dashboard Cite

show abstract

“…There is an analogy with the description of the afferent (sensory) receptors that are thought to cause cough. They have been given many overlapping and somewhat-confusing names: irritant receptors, rapidly adapting receptors, cough receptors, deflation receptors, nociceptors, J-receptors, pulmonary and bronchial C-fibre receptors, Ad nociceptors, but this does not matter greatly because the writers have nearly always clearly defined what they are describing; indeed, the need to define the true cough sensor(s) is stimulating much valuable research [22,23].…”

Section: Cough: What's In a Name?mentioning

confidence: 99%

“…There have been very few records similar to figure 2 in humans, except for the extensive studies by NISHINO and colleagues [2,22]; figures 4 and 5 are taken from these articles. Figure 4 shows the response to application of distilled water to the larynx of a non-anaesthetised subject: there are three ERs followed by a cough (note the deep inspiration) followed by another ER.…”

mentioning

confidence: 99%

Cough: what's in a name?

Widdicombe

Fontana²

2006

Eur Respir J

119

View full text Add to dashboard Cite

The cough reflex (CR) and the expiration reflex (ER) are two defensive reflexes from the respiratory tract, the latter mainly from the larynx. Both are elicited by mechanical and chemical irritation of the airway mucosa, and are a characteristic of airway diseases, but they have different functions. The CR first draws air into the lungs, to accentuate the subsequent expulsive phase; the ER consists of a strong expiration, to prevent aspiration of material into the lungs. They have different sensory pathways, central nervous circuits, and physiological and pharmacological modulations. In practice, coughing often consists of a combination of the two reflexes, a cough bout, epoch or attack. Articles on cough usually do not distinguish between the two reflexes, or whether the coughs are single events or epochs; they usually only measure frequency of expiratory efforts, and neglect other aspects. Current methods for measuring and assessing cough are described, with indications of when the use of these methods may be important.

show abstract

“…This preinspiratory (Pre-I) activity has been suggested to benefit UAW patency by dilating and stiffening the UAW before the onset of I airflow (30). Similar to the HN, the onset of FN, SLN, and RLN I bursting occurs before the onset of phrenic bursting (16,25).…”

mentioning

confidence: 99%

Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat

Lee¹,

Fuller²,

Tung³

et al. 2007

Journal of Applied Physiology

View full text Add to dashboard Cite

Lee K-Z, Fuller DD, Tung L-C, Lu I-J, Ku L-C, Hwang J-C. Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat. J Appl Physiol 102: [878][879][880][881][882][883][884][885][886][887][888][889] 2007. First published November 2, 2006; doi:10.1152/japplphysiol.00934.2006.-Phasic bursting in the hypoglossal nerve can be uncoupled from phrenic bursting by application of positive end-expired pressure (PEEP). We wished to determine whether similar uncoupling can also be induced in other respiratory-modulated upper airway (UAW) motor outputs. Discharge of the facial, hypoglossal, superior laryngeal, recurrent laryngeal, and phrenic nerves was recorded in anesthetized, ventilated rats during stepwise changes in PEEP with a normocapnic, hyperoxic background. Application of 3-to 6-cmH 2O PEEP caused the onset inspiratory (I) UAW nerve bursting to precede the phrenic burst but did not uncouple bursting. In contrast, application of 9-to 12-cmH2O PEEP uncoupled UAW neurograms such that rhythmic bursting occurred during periods of phrenic quiescence. Single-fiber recording experiments were conducted to determine whether a specific population of UAW motoneurons is recruited during uncoupled bursting. The data indicate that expiratory-inspiratory (EI) motoneurons remained active, while I motoneurons did not fire during uncoupled UAW bursting. Finally, we examined the relationship between motoneuron discharge rate and PEEP during coupled UAW and phrenic bursting. EI discharge rate was linearly related to PEEP during preinspiration, but showed no relationship to PEEP during inspiration. Our results demonstrate that multiple UAW motor outputs can be uncoupled from phrenic bursting, and this response is associated with bursting of EI nerve fibers. The relationship between PEEP and EI motoneuron discharge rate differs during preinspiratory and I periods; this may indicate that bursting during these phases of the respiratory cycle is controlled by distinct neuronal outputs. uncoupled activity; motoneurons; expiratory-inspiratory; preinspiratory THE MAMMALIAN UPPER AIRWAY (UAW) consists of the airflow passages extending from the trachea to the external nares and is thus composed of the nasal cavity, pharynx, and larynx (34). The compliance and geometry of this region are influenced by a number of skeletal muscles. Among them are the alae nasi, tongue, and laryngeal muscles, which are innervated by the facial (FN), hypoglossal (HN) and superior (SLN), and recurrent laryngeal nerves (RLN), respectively (1,26,41).Many studies have shown that the inspiratory (I) discharge of the HN precedes the phrenic I burst (5,6,13,17,23,33). This preinspiratory (Pre-I) activity has been suggested to benefit UAW patency by dilating and stiffening the UAW before the onset of I airflow (30). Similar to the HN, the onset of FN, SLN, and RLN I bursting occurs before the onset of phrenic bursting (16,25).The respiratory-related discharge of the UAW muscles is influenced by various chemical and mechanical ...

show abstract

Physiological and Pathophysiological Implications of Upper Airway Reflexes in Humans.

Cited by 106 publications

References 68 publications

Vocal cord dysfunction: what do we know?

Vocal cord dysfunction: what do we know?

Cough: what's in a name?

Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat

Contact Info

Product

Resources

About