Electroencephalographic evidence for a respiratory-related cortical activity specific of the preparation of prephonatory breaths

Tremoureux, Lysandre; Raux, Mathieu; Ranohavimparany, Anja; Morélot-Panzini, Capucine; Pouget, Pierre; Similowski, Thomas

doi:10.1016/j.resp.2014.06.018

Cited by 25 publications

(31 citation statements)

References 66 publications

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“…Resting ventilation is under the control of brainstem automatic neural activity (Feldman, Del Negro, & Gray, ). Healthy humans do not exhibit EEG‐detectable respiratory‐related cortical activity during resting breathing in the sitting position (Dubois et al., ; Launois et al., ; Raux et al., ; Raux, Tremoureux, Couturier, Hug, & Similowski, ; Tremoureux et al., ; Tremoureux et al., , b), and this was confirmed in our subjects. In the present study, we show that moving from the sitting upright to lying supine position induces transient PIPs in half of the non‐obese healthy subjects.…”

Section: Discussionsupporting

confidence: 78%

Postural respiratory‐related cortical activation and rostral fluid shift in awake healthy humans

Launois

Perger

Attali

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Moving to supine induces upper airway modifications and a fluid shift to the neck, which represent inspiratory load that predisposes to upper airway collapse. Is there cortical participation in the response to the load induced by transition to a supine posture in awake healthy subjects? What is the main finding and its importance?Moving to supine induces transient cortical activation in awake healthy subjects, with greater fluid shift, supporting possible cortical participation in the response to upper airway load induced by transition to a supine posture. Our findings open new perspectives in the understanding of the pathogenesis of obstructive sleep apnoea. Abstract Moving from sitting upright to lying supine causes anatomical modifications and a fluid shift to the neck, which represent inspiratory loads that predispose to upper airway collapse. The pre‐inspiratory potential (PIP) corresponds to the cortical activity observed during inspiratory load. In the sitting position during wakefulness, some obstructive sleep apnoea patients exhibit PIP, probably in relationship to upper airway abnormalities. The aim of this study was to investigate whether moving to the supine position induces respiratory‐related cortical activation (PIP) in awake healthy subjects. The ECG was analysed to detect PIP, and EMG activity of the genioglossus muscle and ventilation were measured in the sitting position, immediately after moving to the supine position, and during application of leg positive pressure in the supine position to promote fluid shift, which was measured by bioelectrical impedance. Twenty‐four subjects were included. From sitting to lying, PIP prevalence increased from 1/24 to 11/24 (P = 0.002), and ventilation decreased with no change in genioglossus activity. The fluid shift from sitting to supine was higher in the subjects exhibiting PIP while supine compared with the subjects without PIP [median (25th; 75th centiles) 440 (430; 520) versus 320 (275; 385) ml, P = 0.018], without any other differences. From before to during leg positive pressure, PIP disappeared (P = 0.006). These results indicate that moving from sitting to lying induces transient respiratory‐related cortical activity in awake healthy subjects with greater fluid shift, supporting possible cortical participation in the response to upper airway loading induced by moving from sitting upright to lying supine. This study offers new perspectives in the understanding of obstructive sleep apnoea pathogenesis.

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Section: Discussionsupporting

confidence: 78%

Postural respiratory‐related cortical activation and rostral fluid shift in awake healthy humans

Launois

Perger

Attali

et al. 2019

Experimental Physiology

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“…In addition, higher cortical networks in the motor and premotor regions are involved in the control of breathing during voluntary and involuntary complex actions. The priority of cortical control during quiet relaxed breathing is to allow a coordination between breathing and other motor functions such as speaking [8], mastication, swallowing, or gait. Gait is considered as an automatic function, but under certain conditions, gait control becomes dependent on higher specific cortical regions and cognitive function [9].…”

Section: Control Of Breathingmentioning

confidence: 99%

The Pathophysiology of Respiratory Failure: Control of Breathing, Respiratory Load, and Muscle Capacity

Adler

Janssens²

2018

Respiration

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The purpose of this review is to provide an overview on how interactions between control of breathing, respiratory load, and muscle function may lead to respiratory failure. The mechanisms involved vary according to the underlying pathology, but respiratory failure is most often the result of an imbalance between the muscular pump and the mechanical load placed upon it. Changes in respiratory drive and response to CO₂ seem to be important contributors to the pathophysiology of respiratory failure. Inspiratory muscle dysfunction is also frequent but is not a mandatory prerequisite to respiratory failure since increased load may also be sufficient to precipitate it. It is crucial to recognize these interactions to be able to timeously establish patients on mechanical ventilation and adapt the ventilator settings to their respiratory system physiology.

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“…Darüber hinaus sind höhere kortikale Netzwerke in motorischen und prämotorischen Hirnregionen an der Atmungsregulation im Rahmen willkürlicher und unwillkürlicher komplexer Abläufe beteiligt. Die Priorität der kortikalen Steuerung beim ruhigen, entspannten Atmen ist es, die Koordination zwischen Atmung und anderen motorischen Funktionen wie Sprechen [8], Kauen, Schlucken oder Gehen zu ermöglichen. Gehen gilt als automatische Funktion, doch je nach Umständen können auch übergeordnete spezifische kortikale Regionen und kognitive Funktionen eingreifen [9].…”

Section: Atmungsregulationunclassified

Pathophysiologie der Ateminsuffizienz: Atmungsregulation, Atemlast und Muskelkapazität

Adler¹,

Janssens²

2019

Kompass Pneumol

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Das Ziel dieser Übersichtsarbeit ist es, in Grundzügen darzustellen, wie Wechselwirkungen zwischen der Atmungsregulation, der Atemlast und der Muskelfunktion zu Ateminsuffizienz führen können. Die beteiligten Mechanismen variieren je nach zugrunde liegender Pathologie, aber meist ist eine Ateminsuffizienz das Ergebnis eines Ungleichgewichts zwischen der Muskelpumpe und der auf diese wirkenden mechanischen Belastung. Veränderungen des Atemantriebs und der CO2-Antwort scheinen wichtige Faktoren für die Pathophysiologie der Ateminsuffizienz zu sein. Auch Funktionsstörungen der Einatemmuskeln kommen häufig vor, stellen jedoch keine zwingende Voraussetzung für eine Ateminsuffizienz dar, da diese auch nur durch erhöhte Last herbeigeführt werden kann. Es ist von größter Bedeutung, sich dieser Wechselwirkungen bewusst zu sein, um rechtzeitig eine mechanische Beatmung zu beginnen und ihre Parameter an die individuelle Physiologie des Atmungsapparats des Patienten anzupassen.

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Electroencephalographic evidence for a respiratory-related cortical activity specific of the preparation of prephonatory breaths

Cited by 25 publications

References 66 publications

Postural respiratory‐related cortical activation and rostral fluid shift in awake healthy humans

Postural respiratory‐related cortical activation and rostral fluid shift in awake healthy humans

The Pathophysiology of Respiratory Failure: Control of Breathing, Respiratory Load, and Muscle Capacity

Pathophysiologie der Ateminsuffizienz: Atmungsregulation, Atemlast und Muskelkapazität

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