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Upper Airway Resistance (upper + airway_resistance)

Distribution by Scientific Domains
Medical Sciences50%

Terms modified by Upper Airway Resistance

  • upper airway resistance syndrome
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    Selected Abstracts

    The Kölliker-Fuse nucleus gates the postinspiratory phase of the respiratory cycle to control inspiratory off-switch and upper airway resistance in rat

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2006
    Mathias Dutschmann
    Abstract Lesion or pharmacological manipulation of the dorsolateral pons can transform the breathing pattern to apneusis (pathological prolonged inspiration). Apneusis reflects a disturbed inspiratory off-switch mechanism (IOS) leading to a delayed phase transition from inspiration to expiration. Under intact conditions the IOS is irreversibly mediated via activation of postinspiratory (PI) neurons within the respiratory network. In parallel, populations of laryngeal premotoneurons manifest the IOS by a brief glottal constriction during the PI phase. We investigated effects of pontine excitation (glutamate injection) or temporary lesion after injection of a GABA-receptor agonist (isoguvacine) on the strength of PI-pool activity determined from respiratory motor outputs or kinesiological measurements of laryngeal resistance in a perfused brainstem preparation. Glutamate microinjections into distinct parts of the pontine Kölliker-Fuse nucleus (KF) evoked a tonic excitation of PI-motor activity or sustained laryngeal constriction accompanied by prolongation of the expiratory phase. Subsequent isoguvacine microinjections at the same loci abolished PI-motor or laryngeal constrictor activity, triggered apneusis and established a variable and decreased breathing frequency. In summary, we revealed that excitation or inhibition of defined areas within the KF activated and blocked PI activity and, consequently, IOS. Therefore, we conclude, first, that descending KF inputs are essential to gate PI activity required for a proper pattern formation and phase control within the respiratory network, at least during absence of pulmonary stretch receptor activity and, secondly, that the KF contains large numbers of laryngeal PI premotor neurons that might have a key role in the regulation of upper airway resistance during reflex control and vocalization. [source]

    Bruxism physiology and pathology: an overview for clinicians,

    JOURNAL OF ORAL REHABILITATION, Issue 7 2008
    G. J. LAVIGNE
    Summary, Awake bruxism is defined as the awareness of jaw clenching. Its prevalence is reported to be 20% among the adult population. Awake bruxism is mainly associated with nervous tic and reactions to stress. The physiology and pathology of awake bruxism is unknown, although stress and anxiety are considered to be risk factors. During sleep, awareness of tooth grinding (as noted by sleep partner or family members) is reported by 8% of the population. Sleep bruxism is a behaviour that was recently classified as a ,sleep-related movement disorder'. There is limited evidence to support the role of occlusal factors in the aetiology of sleep bruxism. Recent publications suggest that sleep bruxism is secondary to sleep-related micro-arousals (defined by a rise in autonomic cardiac and respiratory activity that tends to be repeated 8,14 times per hour of sleep). The putative roles of hereditary (genetic) factors and of upper airway resistance in the genesis of rhythmic masticatory muscle activity and of sleep bruxism are under investigation. Moreover, rhythmic masticatory muscle activity in sleep bruxism peaks in the minutes before rapid eye movement sleep, which suggests that some mechanism related to sleep stage transitions exerts an influence on the motor neurons that facilitate the onset of sleep bruxism. Finally, it remains to be clarified when bruxism, as a behaviour found in an otherwise healthy population, becomes a disorder, i.e. associated with consequences (e.g. tooth damage, pain and social/marital conflict) requires intervention by a clinician. [source]

    Laryngeal sensitivity in the neonatal period: From bench to bedside

    PEDIATRIC PULMONOLOGY, Issue 8 2007
    Philippe Reix MD
    Abstract Laryngeal sensitivity in the newborn has been a subject of great interest for both researchers and clinicians for a number of years. From a clinical standpoint, laryngeal sensitivity is essential for both preventing foreign substances from entering into the lower airway and for finely tuning upper airway resistance. However, heightened reflexes originating from the laryngeal receptors in newborns and infants, due to neural immaturity, can lead to potentially dangerous cardiorespiratory events. The latter have been linked to apneas of prematurity, apparent life-threatening events, and sudden infant death syndrome (SIDS). From a physiological standpoint, many mechanisms pertaining to reflexes originating from laryngeal receptors are yet to be fully understood. This short review is an attempt to summarize current knowledge on laryngeal sensitivity and its potential consequences upon control of breathing abnormalities encountered within the first weeks of life. Pediatr Pulmonol. 2007; 42:674,682. © 2007 Wiley-Liss, Inc. [source]