Corticomotor control of the genioglossus in awake OSAS patients: a transcranial magnetic stimulation study

<p>Abstract</p> <p>Background</p> <p>Upper airway collapse does not occur during wake in obstructive sleep apnea patients. This points to wake-related compensatory mechanisms, and possibly to a modified corticomotor control of upper airway dilator muscles. The objectives of the study were to characterize the responsiveness of the genioglossus to transcranial magnetic stimulation during respiratory and non-respiratory facilitatory maneuvers in obstructive sleep apnea patients, and to compare it to the responsiveness of the diaphragm, with reference to normal controls.</p> <p>Methods</p> <p>Motor evoked potentials of the genioglossus and of the diaphragm, with the corresponding motor thresholds, were recorded in response to transcranial magnetic stimulation applied during expiration, inspiration and during maximal tongue protraction in 13 sleep apnea patients and 8 normal controls.</p> <p>Main Results</p> <p>In the sleep apnea patients: 1) combined genioglossus and diaphragm responses occurred more frequently than in controls (<it>P </it>< 0.0001); 2) the amplitude of the genioglossus response increased during inspiratory maneuvers (not observed in controls); 3) the latency of the genioglossus response decreased during tongue protraction (not observed in controls). A significant negative correlation was found between the latency of the genioglossus response and the apnea-hypopnea index; 4) the difference in diaphragm and genioglossus cortico-motor responses during tongue protraction and inspiratory loading differed between sleep apnea and controls.</p> <p>Conclusion</p> <p>Sleep apnea patients and control subjects differ in the response pattern of the genioglossus and of the diaphragm to facilitatory maneuvers, some of the differences being related to the frequency of sleep-related events.</p

Slower Is Higher: Threshold Modulation of Cortical Activity in Voluntary Control of Breathing Initiation

Speech or programmed sentences must often be interrupted in order to listen to and interact with interlocutors. Among many processes that produce such complex acts, the brain must precisely adjust breathing to produce adequate phonation. The mechanism of these adjustments is multifactorial and still poorly understood. In order to selectively examine the adjustment in breath control, we recorded respiratory-related premotor cortical potentials from the scalp of human subjects while they performed a single breathing initiation or inhibition task. We found that voluntary breathing is initiated if, and only if, the cortical premotor potential activity reaches a threshold activation level. The stochastic variability in the threshold correlates to the distribution of initiation times of breathing. The data also fitted a computerized interactive race model. Modeling results confirm that this model is also as effective in respiratory modality, as it has been found to be for eye and hand movements. No modifications were required to account for respiratory cycle inhibition processes. In this overly simplified task, we showed a link between voluntary initiation and control of breathing and activity in a fronto-median region of the cerebral cortex. These results shed light on some of the physiological constraints involved in the complex mechanisms of respiration, phonation, and language

induction non-invasive d'une plasticité de la commande ventilatoire chez l'humain sain

La commande de la ventilation chez l'humain est capable d'adaptation persistante qui repose sur des mécanismes de type LTP. Différentes techniques permettant l'induction de plasticité sont couramment utilisées mais leur application au contrôle ventilatoire n'a fait l'objet que de très peu de travaux.L'objectif de cette thèse est (1) examiner la possibilité d'induire des mécanismes de type LTP par la rTMS et la tsDCS en deux sites de la commande ventilatoire destinée au diaphragme, l'AMS et les métamères C3-C5 ; (2) évaluer les conséquences sur le profil ventilatoire en ventilation de repos et lorsque la ventilation est artificiellement contrainte. Nous avons examiné les effets d'un conditionnement inhibiteur appliqué par rTMS en regard de l'AMS sur l'excitabilité corticophrénique. Nous avons observé la présence d'une diminution persistante de cette excitabilité et en avons tiré la proposition qu'en ventilation de repos l'AMS augmente l'excitabilité de la commande ventilatoire à l'éveil. Nous avons alors considéré les conséquences de la rTMS sur la ventilation expérimentalement contrainte. Les modifications du profil ventilatoire induites par la rTMS sont en faveur d'une participation de l'AMS à la production ou au traitement de la copie d'efférence. Dans une 3ème étude, nous avons examiné les effets de la tsDCS au niveau C3-C5 sur l'excitabilité corticophrénique et sur le profil ventilatoire. L'augmentation de cette excitabilité et du volume courant nous a conduit à suggérer la possibilité d'induire une plasticité respiratoire au niveau spinal.L'ensemble de ces résultats nous permet d'envisager des perspectives thérapeutiques à l'utilisation de la rTMS et de la tsDCS.A salient feature of the ventilatory control system is its ability to persistently adapt its behaviour. This stems from long-term plasticity mechanisms similar to those described for the neural control in general. Plasticity can be induced by various non-invasive stimulation techniques(e.g. rTMS, TDCS, tsDCS) that are commonly used but have not be systematically applied to ventilatory plasticity. The aim of this thesis is twofold: (1) to examine the possibility of inducing LTP by rTMS and tsDCS at two sites of the ventilatory control system, namely the SMA and the phrenic motoneurons: (2) to evaluate the impact of such plasticity on breathing pattern during spontaneous ventilation and inspiratory threshold loading. We examined the effects of an inhibitory rTMS paradigm applied to the SMA on corticophrenic excitability. We observed a persistent decrease in corticophrenic excitability and therefore proposed that the SMA participates in the increased resting state of the ventilatory motor system during wake. Then we considered the consequences of rTMS on breathing pattern during ITL. The corresponding modifications support a contribution of the SMA to the production or processing of an ventilatory efference copy. In a third study, we examined the effects of a tsDCS delivered to C3-C5 on the corticophrenic excitability and on the respiratory pattern. Increased corticophrenic excitability and tidal volume were observed. This suggests that respiratory plasticity takes place at the spinal level. Taken together, these results open the perspective of harnessing respiratory plasticity as a therapeutic tool in disorders altering the ventilatory command.PARIS-JUSSIEU-Bib.électronique (751059901) / SudocSudocFranceF

Diaphragm pacing failure secondary to deteriorated chest wall mechanics: When a good diaphragm does not suffice to take a good breath in

AbstractDiaphragm pacing allows certain quadriplegic patients to be weaned from mechanical ventilation. Pacing failure can result from device dysfunction, neurotransmission failure, or degraded lung mechanics (such as atelectasis). We report two cases where progressive pacing failure was attributed to deteriorated chest wall mechanics. The first patient suffered from cervical spinal cord injury at age 45, was implanted with a phrenic stimulator (intrathoracic), successfully weaned from ventilation, and permanently paced for 7 years. Pacing effectiveness then slowly declined, finally attributed to rib cage stiffening due to ankylosing spondylitis. The second patient became quadriplegic after meningitis at age 15, was implanted with a phrenic stimulator (intradiaphragmatic) and weaned. After a year hypoventilation developed without obvious cause. In relationship with complex endocrine disorders, the patient had gained 31 kg. Pacing failure was attributed to excessive mechanical inspiratory load. Rib cage mechanics abnormalities should be listed among causes of diaphragm pacing failure and it should be kept in mind that a “good diaphragm” is not sufficient to produce a “good inspiration”

Physiological Validation of an Airborne Ultrasound Based Surface Motion Camera for a Contactless Characterization of Breathing Pattern in Humans

Characterizing the breathing pattern in naturally breathing humans brings important information on respiratory mechanics, respiratory muscle, and breathing control. However, measuring breathing modifies breathing (observer effect) through the effects of instrumentation and awareness: measuring human breathing under true ecological conditions is currently impossible. This study tested the hypothesis that non-contact vibrometry using airborne ultrasound (SONAR) could measure breathing movements in a contactless and invisible manner. Thus, first, we evaluated the validity of SONAR measurements by testing their interchangeability with pneumotachograph (PNT) measurements obtained at the same time. We also aimed at evaluating the observer effect by comparing breathing variability obtained by SONAR versus SONAR-PNT measurements. Twenty-three healthy subjects (12 men and 11 women; mean age 33 years – range: 20–54) were studied during resting breathing while sitting on a chair. Breathing activity was described in terms of ventilatory flow measured using a PNT and, either simultaneously or sequentially, with a SONAR device measuring the velocity of the surface motion of the chest wall. SONAR was focused either anteriorly on the xiphoid process or posteriorly on the lower part of the costal margin. Discrete ventilatory temporal and volume variables and their coefficients of variability were calculated from the flow signal (PNT) and the velocity signal (SONAR) and tested for interchangeability (Passing-Bablok regression). Tidal volume (VT) and displacement were linearly related. Breathing frequency (BF), total cycle time (TT), inspiratory time (TI), and expiratory time (TE) met interchangeability criteria. Their coefficients of variation were not statistically significantly different with PNT and SONAR-only. This was true for both the anterior and the posterior SONAR measurements. Non-contact vibrometry using airborne ultrasound is a valid tool for measuring resting breathing pattern

Comparison of bedside measurement of cardiac output with the thermodilution method and the Fick method in mechanically ventilated patients

INTRODUCTION: Bedside cardiac output determination is a common preoccupation in the critically ill. All available methods have drawbacks. We wished to re-examine the agreement between cardiac output determined using the thermodilution method (QTTHERM) and cardiac output determined using the metabolic (Fick) method (QTFICK) in patients with extremely severe states, all the more so in the context of changing practices in the management of patients. Indeed, the interchangeability of the methods is a clinically relevant question; for instance, in view of the debate about the risk–benefit balance of right heart catheterization. PATIENTS AND METHODS: Eighteen mechanically ventilated passive patients with a right heart catheter in place were studied (six women, 12 men; age, 39–84 years; simplified acute physiology scoreII, 39–111). QTTHERM was obtained using a standard procedure. QTFICK was measured from oxygen consumption, carbon dioxide production, and arterial and mixed venous oxygen contents. Forty-nine steady-state pairs of measurements were performed. The data were normalized for repeated measurements, and were tested for correlation and agreement. RESULTS: The QTFICK value was 5.2 ± 2.0 l/min whereas that of QTTHERM was 5.8 ± 1.9 l/min (R = 0.840, P < 0.0001; mean difference, -0.7 l/min; lower limit of agreement, -2.8 l/min; upper limit of agreement, 1.5 l/min). The agreement was excellent between the two techniques at QTTHERM values <5 l/min but became too loose for clinical interchangeability above this value. Tricuspid regurgitation did not influence the results. DISCUSSION AND CONCLUSIONS: No gold standard is established to measure cardiac output in critically ill patients. The thermodilution method has known limitations that can lead to inaccuracies. The metabolic method also has potential pitfalls in this context, particularly if there is increased oxygen consumption within the lungs. The concordance between the two methods for low cardiac output values suggests that they can both be relied upon for clinical decision making in this context. Conversely, a high cardiac output value is more difficult to rely on in absolute terms