478 research outputs found
sj-pdf-1-pmj-10.1177_02692163221118198 – Supplemental material for ‘You can’t feel what we feel’: Multifaceted dyspnoea invisibility in advanced chronic obstructive pulmonary disease examined through interpretative phenomenological analysis
No full textSupplemental material, sj-pdf-1-pmj-10.1177_02692163221118198 for ‘You can’t feel what we feel’: Multifaceted dyspnoea invisibility in advanced chronic obstructive pulmonary disease examined through interpretative phenomenological analysis by Laure Serresse, Antoine Guerder, Jonathan Dedonder, Nathalie Nion, Sophie Lavault, Capucine Morélot-Panzini, Jésus Gonzalez-Bermejo, Laelia Benoit and Thomas Similowski in Palliative Medicine</p
sj-html-2-pmj-10.1177_02692163221118198 – Supplemental material for ‘You can’t feel what we feel’: Multifaceted dyspnoea invisibility in advanced chronic obstructive pulmonary disease examined through interpretative phenomenological analysis
No full textSupplemental material, sj-html-2-pmj-10.1177_02692163221118198 for ‘You can’t feel what we feel’: Multifaceted dyspnoea invisibility in advanced chronic obstructive pulmonary disease examined through interpretative phenomenological analysis by Laure Serresse, Antoine Guerder, Jonathan Dedonder, Nathalie Nion, Sophie Lavault, Capucine Morélot-Panzini, Jésus Gonzalez-Bermejo, Laelia Benoit and Thomas Similowski in Palliative Medicine</p
Comparison of magnetic and electrical phrenic nerve stimulation in assessment of phrenic nerve conduction time
No full text Similowski, Thomas, Selma Mehiri, Alexandre Duguet, Valérie Attali, Christian Straus, and Jean-Philippe Derenne.Comparison of magnetic and electrical phrenic nerve stimulation in assessment of phrenic nerve conduction time. J. Appl. Physiol. 82(4): 1190–1199, 1997.—Cervical magnetic stimulation (CMS), a nonvolitional test of diaphragm function, is an easy means for measuring the latency of the diaphragm motor response to phrenic nerve stimulation, namely, phrenic nerve conduction time (PNCT). In this application, CMS has some practical advantages over electrical stimulation of the phrenic nerve in the neck (ES). Although normal ES-PNCTs have been consistently reported between 7 and 8 ms, data are less homogeneous for CMS-PNCTs, with some reports suggesting lower values. This study systematically compares ES- and CMS-PNCTs for the same subjects. Surface recordings of diaphragmatic electromyographic activity were obtained for seven healthy volunteers during ES and CMS of varying intensities. On average, ES-PNCTs amounted to 6.41 ± 0.84 ms and were little influenced by stimulation intensity. With CMS, PNCTs were significantly lower (average difference 1.05 ms), showing a marked increase as CMS intensity lessened. ES and CMS values became comparable for a CMS intensity 65% of the maximal possible intensity of 2.5 Tesla. These findings may be the result of phrenic nerve depolarization occurring more distally than expected with CMS, which may have clinical implications regarding the diagnosis and follow-up of phrenic nerve lesions. </jats:p
Counter-irritation phenomenon to study neurophysiological mechanisms of dyspnea : from physiology to therapeutic
No full textL'existence d'une contre-irritation dyspnée-douleur, c'est-à-dire l'inhibition d'une sensation douloureuse par une sensation de dyspnée, permet d'établie une analogie forte dyspnée - douleur. La dyspnée de type " effort inspiratoire excessif " inhibe le réflexe spinal de flexion, ce qui indique qu'elle est au moins en partie médiée par des fibres C. Cette thèse approfondit les connaissances dans ce domaine. Elle montre que la dyspnée de type soif d'air possède des propriétés analgésiques procédant de mécanismes centraux puisqu'elle interagit avec les potentiels évoqués laser qui sont le reflet des mécanismes corticaux mis en jeu au cours de stimulation douloureuse. Elle évalue l'effet d'un antalgique non opioïde de pallier 1, le nefopam, sur une dyspnée expérimentale de type " effort inspiratoire excessif " sans mettre en évidence d'interaction du nefopam avec la contre-irritation dyspnée douleur.Dyspnea – pain counter – irritation, namely the inhibition of nociceptive sensation by dyspneic sensation, indicates that dyspnea and pain share some mechanisms. Dyspnea of the work/effort type inhibits the spinal flexion reflex, meaning that it involves C-Fibers. This thesis aims at improving knowledge in this field. It shows that dyspnea of the air hunger type has analgesics properties proceeding from central mechanisms: “air hunger” indeed inhibits laser evoked potentials that depends on the pain-related activation of cortical networks. It also evaluates the effect of a non-opioid first step analgesic, nefopam, on an experimental dyspnea of the “work-effort” type, and shows that although nefopam acts on C-fibers, it does not attenuate dyspnea and does not modify dyspnea-pain counter-irritation as evaluated by laser-evoked potentials. Finally, the thesis brings the first evidence of dyspnea-pain interactions in the clinical setting, by showing that ALS patients treated by non-invasive ventilation exhibit heightened pain sensitivity concomitant to the relief of dyspnea. These data advance the current understanding of dyspnea mechanisms and open new perspectives for treatment evaluation
Upper airways stability and central integration
No full textLe syndrome des apnées obstructives du sommeil (SAOS) est caractérisé par des épisodes répétitifs de collapsus des voies aériennes supérieures (VAS) durant le sommeil. Au cours du SAOS les propriétés mécaniques des voies aériennes supérieures sont altérées, dans le sens d'une réduction de leur capacité à laisser passer l'air, ce qui peut être assimilé à une "charge" inspiratoire. Les apnées obstructives ne se produisent jamais à l'éveil, suggérant qu'il existe, des mécanismes protecteurs d'origine corticale, de type " compensation de charge ", liés à l'éveil. Ce travail permis de caractériser ces mécanismes chez le sujet sain et le patient SAOS. Une première étude a décrit la relation pression/débit des VAS à l'éveil afin d'approcher le phénomène de compensation de charge, avant et après un traitement modulant le contrôle neurovégétatif des VAS par la compression du ganglion ptérygopalatin. La deuxième étude a mis en évidence à l'éveil chez les patients SAOS, une activité corticale motrice liée à la respiration (présence de potentiels électroencephalographiques - PPI), dont l'origine semble liée à la dysfonction des VAS, et qui est susceptible d'expliquer l'augmentation du niveau de contrôle respiratoire central connu dans le SAOS. La troisième étude a mis en évidence un phénomène de filtrage des sensations respiratoires à l'éveil chez des patients SAOS, avec restauration des ces sensations sous orthèse d'avancée mandibulaire, permettant de relier l'amélioration des propriétés mécaniques des VAS à l'intégration centrale des sensations respiratoires. Enfin la relation pression/débit a fait l'objet de deux modélisations.The obstructive sleep apnoea syndrome (OSAS) involves recurrent sleep-related upper airways (UA) collapse. UA mechanical properties and neural control are altered imposing a mechanical load on inspiration. UA collapse does not occur during wakefulness, hence arousal-dependent compensation. Three studies in healthy and apnoeic patients allowed characterizing it. From upper-airway pressure-flow relationships, the first study described local compensation mechanisms, before and after a neurovegetative modulation based on ptérygopalatin node compression. The second study showed a respiratory-related cortical activity that could contribute to the increased neural drive to upper airway and to inspiratory muscles that has previously been described in OSAS, and could therefore contribute to the arousal-dependent compensation of upper airway abnormalities. The third study showed a sensory gating-out process of breathing sensations in OSAS that could be reversed by mandibular advancement device, allowing linking upper-airway stability improvement to central integration of respiratory sensations. Finally, upper-airway pressure-flow relationship was approached by two models
The best peak expiratory flow is flow-limited and effort independent in normal subjects.
No full textBench Evaluation of Four Portable Oxygen Concentrators Under Different Conditions Representing Altitudes of 2438, 4200, and 8000 m
No full textInternational audienceBunel, Vincent, Amr Shoukri, Frederic Choin, Serge Roblin, Cindy Smith, Thomas Similowski, Capucine Morélot-Panzini, and Jésus Gonzalez. Bench evaluation of four portable oxygen concentrators under different conditions representing altitudes of 2438, 4200, and 8000 m. High Alt Med Biol. 17:370–374, 2016.—Air travel is responsible for a reduction of the partial pressure of oxygen (O2) as a result of the decreased barometric pressure. This hypobaric hypoxia can be dangerous for passengers with respiratory diseases, requiring initiation or intensification of oxygen therapy during the flight. In-flight oxygen therapy can be provided by portable oxygen concentrators, which are less expensive and more practical than oxygen cylinders, but no study has evaluated their capacity to concentrate oxygen under simulated flight conditions. We tested four portable oxygen concentrators during a bench test study. The O2 concentrations (FO2) produced were measured under three different conditions: in room air at sea level, under hypoxia due to a reduction of the partial pressure of O2 (normobaric hypoxia, which can be performed routinely), and under hypoxia due to a reduction of atmospheric pressure (hypobaric hypoxia, using a chamber manufactured by Airbus Defence and Space). The FO2 obtained under conditions of hypobaric hypoxia (chamber) was lower than that measured in room air (0.92 [0.89–0.92] vs. 0.93 [0.92–0.94], p = 0.029), but only one portable oxygen concentrator was unable to maintain an FO2 ≥ 0.90 (0.89 [0.89–0.89]). In contrast, under conditions of normobaric hypoxia (tent) simulating an altitude of 2438 m, none of the apparatuses tested was able to achieve an FO2 greater than 0.76. (0.75 [0.75–0.76] vs. 0.93 [0.92–0.94], p = 0.029). Almost all portable oxygen concentrators were able to generate a sufficient quantity of O2 at simulated altitudes of 2438 m and can therefore be used in the aircraft cabin. Unfortunately, verification of the reliability and efficacy of these devices in a patient would require a nonroutinely available technology, and no preflight test can currently be performed by using simple techniques such as hypobaric hypoxia
Neurophysiological properties of the upper airway during wakefulness in healthy subject and in patient with obstructive sleep apnea syndrome : influence of the supine position
No full textLe syndrome d’apnées obstructives du sommeil (SAOS) se caractérise par un collapsus répété des voies aériennes supérieures (VAS) durant le sommeil. Il résulte d’anomalies anatomiques des VAS qui constituent une charge inspiratoire et d’un défaut de réponse neuromusculaire à cette charge durant le sommeil. A l’éveil, il n’y a jamais de collapsus des VAS ce qui suggère l’existence de mécanismes compensatoires. Cette thèse explore ces mécanismes en étudiant la réponse à la charge imposée par le décubitus dorsal chez des sujets sains et des patients SAOS à l’éveil. Nous retrouvons chez 42% des patients SAOS éveillés en position assise une activité corticale liée à la ventilation (potentiels pré-inspiratoires, PPI) qui est absente chez les sujets sains (étude 1) et qui pourrait traduire une augmentation de la commande ventilatoire en réponse aux anomalies des VAS. Le passage en décubitus dorsal s’accompagne de l’apparition d’un PPI chez 46% des sujets sains vraisemblablement en lien avec une augmentation de la charge liée au déplacement de liquides des membres inférieurs vers la région cervicale (étude 2). A l’inverse, chez les patients SAOS, le décubitus dorsal est associé à une diminution significative de l’incidence des PPI mais à une augmentation de l’activité du génioglosse, muscle dilatateur des VAS (étude 3), probablement réflexe à une augmentation de la pression négative pharyngée générée par la charge imposée par le décubitus. Ces données montrent une réponse corticale différente des sujets sains et des patients SAOS face à la charge induite par le décubitus dorsal, ce qui contribue à mieux comprendre le contrôle des VAS et la physiopathologie du SAOS.The obstructive sleep apnea syndrome (OSAS) is characterized by recurrent upper airway (UA) collapse during sleep. It involves UA anatomical abnormalities accompanied by increased inspiratory load and defect in compensatory neuromuscular response to this load during sleep. UA collapse does not occur during wakefulness, suggesting that wakefulness-dependant neuromuscular response compensates for the increased inspiratory load. This thesis investigates these compensatory mechanisms by studying the response to the load imposed by the supine position in healthy subjects and OSAS patients during wakefulness. We found in 42% of awake OSAS patients studied in sitting position, a respiratory-related cortical activity (pre-inspiratory potentials, PIP). This activity was absent in healthy subjects (study 1) and could correspond to an increased neural drive in response to UA abnormalities. Moving to supine position was associated with the occurrence of PIP in 46% of healthy subjects probably related to an increase in fluid shift from the legs to the neck (study 2). Conversely, in OSAS patients, supine position was associated with a significant decrease in the incidence of PIP but with an increase in the genioglossus activity, an UA dilator muscle, (study 3), probably reflex to the increase in pharyngeal negative pressure induced by the load imposed by supine position. These data show a different cortical response of healthy subjects and OSAS patients to an increased load induced by supine position. It contributes to better understand the respiratory control of UA and the pathophysiology of OSAS
Breathing - cognition interactions and cognitive consequences of a cortical ventilatory drive over activation : study in healthy subjects and Congenital Central Hypoventilation Syndrome patients
No full textUne commande ventilatoire d’origine corticale peut exister, par exemple lorsque la ventilation est contrainte par des charges mécaniques ou bien lorsque le contrôle automatique est défaillant, comme dans le syndrome d’hypoventilation alvéolaire central congénital (SHACC). L’objectif de ce travail a été de mettre en évidence une compétition de ressources corticales entre ventilation et performances cognitives chez : 1- Des sujets sains soumis à des contraintes ventilatoires mécaniques; 2- Des patients souffrant du SHACC, en ventilation spontanée à l’éveil (VS). 25 sujets sains et 7 patients porteurs de SHACC ont été étudiés à l'aide de tests neuropsychologiques. Chez les sujets sains, ces tests étaient réalisés en ventilation libre et pendant l'application d'une contrainte ventilatoire. Chez les patients, ils ont été réalisés en VS et avec l’appareillage d’assistance ventilatoire du patient. L'impact des différentes conditions a été évalué par l’analyse de la ventilation, celle de la connectivité corticale et des potentiels pré-inspiratoires, et par un questionnaire d’évaluation de la dyspnée. Chez les sujets sains, la ventilation contrainte a induit une modification du profil ventilatoire, une dyspnée et une activation corticale. Elle était associée à une détérioration des tests neurocognitifs mobilisant les capacités attentionnelles. Chez les patients, la VS entraînait une activation corticale associée, au cours des tests, à des désaturations en oxygène, une augmentation de la variabilité respiratoire et des apnées. Il existe donc une compétition entre cognition et ventilation, lorsque cette dernière dépend de la commande corticale.In humans, the ventilatory drive can arise from cortical structures. This cortical control is responsible in healthy subjects for the compensation of mechanical inspiratory loading. In patients with congenital central hypoventilation syndrome (CCHS), the cortical ventilatory drive is involved in compensating the inefficient automatic command. The aim of this study was to demonstrate a competition between cerebral resources leading to impaired cognitive performances and/or altered ventilation in: 1- healthy subjects submitted to inspiratory threshold loading (ITL); and 2 – CCHS patients during spontaneous breathing (SB). Twenty-five healthy subjects and seven CCHS patients were studied using neuropsychological tests. In healthy subjects, the tests were performed during SB and while subjects were breathing against the ITL. In CCHS patients, tests were performed during SB and while patients were breathing with their own ventilatory support. The impact of different conditions was studied by ventilatory recordings and cortical connectivity and pre-inspiratory potential analyses. Dyspnea was evaluated using the Multidimensional Dyspnea Profile questionnaire (MDP). In healthy subjects, breathing against the ITL induced breathing pattern modifications, dyspnea and cortical activation. It was associated to decreased performances tests evaluating attention capacities. In patients, SB led to cortical activation associated to desaturations, and an increase in breathing variability and in apnea frequency during neuropsychological tests. We demonstrated a competition between cognition and ventilation when the latter is depending on cortical resources
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