Assessment of upper airway stabilizing forces with the use of phrenic nerve stimulation in conscious humans.

Phrenic nerve stimulation (PNS) applied at end-expiration allows the investigation of passive upper airway (UA) dynamic during wakefulness. Assuming that phasic UA dilating/stabilizing forces should modify the UA properties when twitches are applied during inspiration, we compared the UA dynamic responses to expiratory and inspiratory twitches (2 s and 200 ms after expiratory and inspiratory onset, respectively) in nine men (mean age 28 yr). This procedure was repeated with a 2-cm mouth opening provided with a closed mouthpiece. The percentage of flow-limited (FL) twitches was significantly higher when PNS was realized during expiration than during inspiration. Maximal inspiratory flow (Vi(max)) of FL twitches was significantly higher for inspiratory twitches (1,383 +/- 42 and 1,185 +/- 40 ml/s). With mouth aperture, Vi(max) decreased with an increase in the corresponding pharyngeal resistance values, and the percentage of twitch with a FL regimen increased but only for inspiratory twitches. We conclude that 1) UA dynamics are significantly influenced by the inspiratory/expiratory timing at which PNS is applied, 2) the improvement in UA dynamic properties observed from expiratory to inspiratory PNS characterizes the overall inspiratory stabilizing effects, and 3) mouth aperture alters the stability of UA structures during inspiration.     

Discriminative power of phrenic twitch-induced dynamic response for diagnosis of sleep apnea during wakefulness.

The diagnosis of the obstructive sleep apnea syndrome relies on polysomnography. Bilateral anterior magnetic phrenic stimulation (BAMPS) mimics the dissociation between upper airway (UA) muscles and diaphragm commands that leads to UA closure during sleep. We evaluated BAMPS as a mean to identify obstructive sleep apnea syndrome patients through the characterization of the UA dynamics in 28 consecutive awake patients (18 apneic and 10 nonapneic). Driving pressure (Pd) and instantaneous flow (V) were recorded in response to BAMPS to determine the point of flow limitation (Vimax) and of minimal flow (Vimin) and the flow-pressure relationship [Vi = (k(1) x Pd) + (k(2) x Pd(2))]. Vimax, Vimin, UA resistance at Vi(min), and the coefficient of the flow-pressure relationship (k(1)) were correlated with apnea-hypopnea index (respectively, R = -0.735, P < 0.0001; R = -0.584, P = 0.001; R = 0.474, P = 0.01; and R = -0.567, P < 0.01). Body mass index was also correlated with apnea-hypopnea index (R = 0.500, P < 0.01). Apneic patients had a lower Vimax (Vimax = 678 +/- 386 vs. 1,247 +/- 271 ml/s; P < 0.001), a lower Vimin (Vimin = 460 +/- 313 vs. 822 +/- 393 ml/s; P < 0.05) and a lower k(1) (k(1) = 162 +/- 67 vs. 272 +/- 112 ml x cmH(2)O x s(-1); P < 0.01) than nonapneic ones. Using a classification and regression tree approach, we found that a Vimax of <803 ml/s (n = 12) selected only apneic patients. When Vimax of >803 ml/s (n = 16), a k(1) of >266.7 ml. cmH(2)O x s(-1) identified only nonapneic patients (n = 5). In 11 cases, Vimax > 803 ml/s and k(1) < 266.7 ml. cmH(2)O x s(-1). These included five nonapneic and six apneic patients. We conclude that UA dynamic properties studied with BAMPS during wakefulness significantly differ between nonapneic and apneic patients.     

Effects of inspiratory diaphragmatic descent on inferior vena caval venous return.

To explain the contradictory results in the literature regarding the effects of inspiratory diaphragmatic descent on inferior vena caval (IVC) venous return, we evaluated changes in total IVC flow as well as regional splanchnic and nonsplanchnic IVC flows by use of ultrasound flow probes placed around the thoracic and subhepatic abdominal IVC during phrenic nerve stimulation (PNS) in anesthetized open-chest dogs. With the abdomen closed (n = 6), PNS under hypervolemic conditions increased the total IVC flow by enhancing the splanchnic IVC flow, with a transient decrease in the nonsplanchnic IVC flow (P less than 0.05). Under hypovolemic conditions, PNS initially increased the total IVC flow but later decreased the total IVC flow by reducing the nonsplanchnic IVC flow, associated with a venous pressure gradient in the IVC across the diaphragm (P less than 0.05), consistent with development of a vascular waterfall. With the abdomen widely open, the mobile abdominal contents eviscerated, and the subhepatic IVC occluded (n = 5), PNS increased the splanchnic IVC flow associated only with an increase in focal contact pressure over the liver without any increase in general abdominal pressure (Pab) (P less than 0.05). These results suggest that our previously proposed concept of abdominal vascular zone conditions (J. Appl. Physiol. 69: 1961-1972, 1990) is useful as a global approximation to understand the effects of respiratory-induced changes in Pab's on the total and regional IVC venous return. Nonhomogeneous distribution of Pab's during diaphragmatic descent may need to be considered to explain all aspects of the behavior of the intact IVC system.     

Influences of head positions and bite opening on collapsibility of the passive pharynx.

A collapsible tube surrounded by soft material within a rigid box was proposed as a two-dimensional mechanical model for the pharyngeal airway. This model predicts that changes in the box size (pharyngeal bony enclosure size anatomically defined as cross-sectional area bounded by the inside edge of bony structures such as the mandible, maxilla, and spine, and being perpendicular to the airway) influence patency of the tube. We examined whether changes in the bony enclosure size either with head positioning or bite opening influence collapsibility of the pharyngeal airway. Static mechanical properties of the passive pharynx were evaluated in anesthetized, paralyzed patients with sleep-disordered breathing before and during neck extension with bite closure (n = 11), neck flexion with bite closure (n = 9), and neutral neck position with bite opening (n = 11). Neck extension significantly increased maximum oropharyngeal airway size and decreased closing pressures of the velopharynx and oropharynx. Notably, neck extension significantly decreased compliance of the oropharyngeal airway wall. Neck flexion and bite opening decreased maximum oropharyngeal airway size and increased closing pressure of the velopharynx and oropharynx. Our results indicate the importance of neck and mandibular position for determining patency and collapsibility of the passive pharynx.     

The effect of static neck flexion on mechanical and neuromuscular behaviors of the cervical spine

Occupations that involve sustained or repetitive neck flexion are associated with a higher incidence of neck pain. Little in vivo information is available on the impact of static neck flexion on cervical spinal tissue. The aim of this study was to assess changes in mechanical and neuromuscular behaviors to sustained neck flexion in healthy adults. Sixty healthy subjects aged 20–35 years participated in this study. The participants were exposed to static neck flexion at a fixed angle of full flexion for 10 min. Mechanical and neuromuscular responses of the cervical spine to sudden perturbations were measured pre- and post-exposure. Magnitude of load-relaxation during flexion exposure, stiffness, peak head angular velocity, and reflexive activities of cervical muscles were recorded. Effective neck stiffness decreased significantly, especially in female participants (P = 0.0001). The reflexive response of the cervical erector spinae muscles to head perturbation delayed significantly (P = 0.0001). Peak head angular velocity was significantly increased after exposure to neck flexion for 10 min, especially in female participants (P = 0.001). In the present study, static flexion resulted in changes in mechanical and neuromuscular behavior of the cervical spine, potentially leading to decreased stiffness of the cervical spine. The results confirm the importance of maintaining a correct head and neck position during work and improving the work environment to reduce the cervical spinal load and work-related neck pain.     

Control of respiratory activity of the genioglossus muscle in micrognathic infants

The genioglossus (GG) muscle activity of four infants with micrognathia and obstructive sleep apnea was recorded to assess the role of this tongue muscle in upper airway maintenance. Respiratory air flow, esophageal pressure, and intramuscular GG electromyograms (EMG) were recorded during wakefulness and sleep. Both tonic and phasic inspiratory GG-EMG activity was recorded in each of the infants. On occasion, no phasic GG activity could be recorded; these silent periods were unassociated with respiratory embarrassment. GG activity increased during sigh breaths. GG activity also increased when the infants spontaneously changed from oral to nasal breathing and, in two infants, with neck flexion associated with complete upper airway obstruction, suggesting that GG-EMG activity is influenced by sudden changes in upper airway resistance. During sleep, the GG-EMG activity significantly increased with 5% CO2 breathing (P less than or equal to 0.001). With nasal airway occlusion during sleep, the GG-EMG activity increased with the first occluded breath and progressively increased during the subsequent occluded breaths, indicating mechanoreceptor and suggesting chemoreceptor modulation. During nasal occlusion trials, there was a progressive increase in phasic inspiratory activity of the GG-EMG that was greater than that of the diaphragm activity (as reflected by esophageal pressure excursions). When pharyngeal airway closure occurred during a nasal occlusion trial, the negative pressure at which the pharyngeal airway closed (upper airway closing pressure) correlated with the GG-EMG activity at the time of closure, suggesting that the GG muscle contributes to maintaining pharyngeal airway patency in the micrognathic infant.     

Breathing route influences upper airway muscle activity in awake normal adults

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21-38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.     

Hypopharyngeal and neck cross-sectional changes monitored by inductive plethysmography

We present a method to assess cross-sectional area (CSA) changes of the extrathoracic airways (EA) by using an inductive plethysmograph (IP) band placed around the upper part of the neck. Measurements of mouth pressure (Pm) (or flow rate, V) and neck CSA changes during respiratory efforts against a high (or infinite) resistance have shown a highly significant relationship between Pm changes (or V changes, respectively), reflecting CSA changes of the EA and CSA changes of the neck. Simultaneous measurements of CSA of the neck (by IP) and of EA (by computerized tomography) during sustained inspiratory and expiratory efforts against a closed airway showed a high correlation between changes in the former and latter structures. Changes in CSA of the neck were larger with positive than negative transmural pressures, in keeping with the known larger compliance of this airway during expiration. We found this method helpful to assess the behavior of the EA during obstructive apnea episodes, hypopneas, and snoring.     

Upper airway extraluminal tissue pressure fluctuations during breathing in rabbits.

Transmural pressure at any level in the upper airway is dependent on the difference between intraluminal airway and extraluminal tissue pressure (ETP). We hypothesized that ETP would be influenced by topography, head and neck position, resistive loading, and stimulated breathing. Twenty-eight male, New Zealand White, anesthetized, spontaneously breathing rabbits breathed via a face mask with attached pneumotachograph to measure airflow and pressure transducer to monitor mask pressure. Tidal volume was measured via integration of the airflow signal. ETP was measured with a pressure transducer-tipped catheter inserted in the tissues of the lateral (ETPlat, n = 28) and anterior (ETPant, n = 21) pharyngeal wall. Head position was controlled at 30, 50, or 70 degrees, and the effect of addition of an external resistor, brief occlusion, or stimulated breathing was examined. Mean ETPlat was approximately 0.7 cmH2O greater than mean ETPant when adjusted for degree of head and neck flexion (P < 0.05). Mean, maximum, and minimum ETP values increased significantly by 0.7-0.8 cmH2O/20 degrees of head and neck flexion when adjusted for site of measurement (P < 0.0001). The main effect of resistive loading and occlusion was an increase in the change in ETPlat (maximum - minimum ETPlat) and change in ETPant at all head and neck positions (P < 0.05). Mean ETPlat and ETPant increased with increasing tidal volume at head and neck position of 30 degrees (all P < 0.05). In conclusion, ETP was nonhomogeneously distributed around the upper airway and increased with both increasing head and neck flexion and increasing tidal volume. Brief airway occlusion increased the size of respiratory-related ETP fluctuations in upper airway ETP.     

Changes in lung volume and upper airway using MRI during application of nasal expiratory positive airway pressure in patients with sleep-disordered breathing

Nasal expiratory positive airway pressure (nEPAP) delivered with a disposable device (Provent, Ventus Medical) has been shown to improve sleep-disordered breathing (SDB) in some subjects. Possible mechanisms of action are 1) increased functional residual capacity (FRC), producing tracheal traction and reducing upper airway (UA) collapsibility, and 2) passive dilatation of the airway by the expiratory pressure, carrying over into inspiration. Using MRI, we estimated change in FRC and ventilation, as well as UA cross-sectional area (CSA), in awake patients breathing on and off the nEPAP device. Ten patients with SDB underwent nocturnal polysomnography and MRI with and without nEPAP. Simultaneous images of the lung and UA were obtained at 6 images/s. Image sequences were obtained during mouth and nose breathing with and without the nEPAP device. The nEPAP device produced an end-expiratory pressure of 4-17 cmH(2)O. End-tidal Pco(2) rose from 39.7 ± 5.3 to 47.1 ± 6.0 Torr (P < 0.01). Lung volume changes were estimated from sagittal MRI of the right lung. Changes in UA CSA were calculated from transverse MRI at the level of the pharynx above the epiglottis. FRC determined by MRI was well correlated to FRC determined by N(2) washout (r = 0.76, P = 0.03). nEPAP resulted in a consistent increase in FRC (46 ± 29%, P < 0.001) and decrease in ventilation (50 ± 15%, P < 0.001), with no change in respiratory frequency. UA CSA at end expiration showed a trend to increase. During wakefulness, nEPAP caused significant hyperinflation, consistent with an increase in tracheal traction and a decrease in UA collapsibility. Direct imaging effects on the UA were less consistent, but there was a trend to dilatation. Finally, we showed significant hypoventilation and rise in Pco(2) during use of the nEPAP device during wakefulness and sleep. Thus, at least three mechanisms of action have the potential to contribute to the therapeutic effect of nEPAP on SDB.     

Sympathetic responses to head-down rotations in humans.

Muscle sympathetic nerve activity (MSNA) increases with head-down neck flexion (HDNF). The present study had three aims: 1) to examine sympathetic and vascular responses to two different magnitudes of HDNF; 2) to examine these same responses during prolonged HDNF; and 3) to determine the influence of nonspecific pressure receptors in the head on MSNA. The first experiment tested responses to two static head positions in the vertical axis [HDNF and intermediate HDNF (I-HDNF; approximately 50% of HDNF)]. MSNA increased above baseline during both I-HDNF and HDNF (from 219 +/- 36 to 301 +/- 47 and from 238 +/- 42 to 356 +/- 59 units/min, respectively; P < 0.01). Calf blood flow (CBF) decreased and calf vascular resistance increased during both I-HDNF and HDNF (P < 0.01). Both the increase in MSNA and the decrease in CBF were linearly related to the magnitude of the downward head rotations (P < 0.01). The second experiment tested responses during prolonged HDNF. MSNA increased (from 223 +/- 63 to 315 +/- 79 units/min; P < 0.01) and CBF decreased (from 3.2 +/- 0.4 to 2.6 +/- 0.04 ml. 100 ml-1. min-1; P < 0.01) at the onset of HDNF. These responses were maintained throughout the 30-min period. Mean arterial blood pressure gradually increased during the 30 min of HDNF (from 94 +/- 4 to 105 +/- 3 mmHg; P < 0.01). In a third experiment, head-down neck extension was performed with subjects in the supine position. Unlike HDNF, head-down neck extension did not affect MSNA. The results from these studies demonstrate that MSNA: 1) increases in magnitude as the degree of HDNF increases; 2) remains elevated above baseline during prolonged HDNF; and 3) responses during HDNF are not associated with nonspecific receptors in the head activated by increases in cerebral pressure.     

Respiratory muscle strength training with nonrespiratory maneuvers.

The diaphragm and abdominal muscles can be recruited during nonrespiratory maneuvers. With these maneuvers, transdiaphragmatic pressures are elevated to levels that could potentially provide a strength-training stimulus. To determine whether repeated forceful nonrespiratory maneuvers strengthen the diaphragm, four healthy subjects performed sit-ups and biceps curls 3-4 days/wk for 16 wk and four subjects served as controls. The maximal transdiaphragmatic pressure was measured at baseline and after 16 wk of training. Maximum static inspiratory and expiratory mouth pressures and diaphragm thickness derived from ultrasound were measured at baseline and 8 and 16 wk. After training, there were significant increases in diaphragm thickness [2.5 +/- 0.1 to 3.2 +/- 0.1 mm (mean +/- SD) (P < 0.001)], maximal transdiaphragmatic pressure [198 +/- 21 to 256 +/- 23 cmH2O (P < 0.02)], maximum static inspiratory pressure [134 +/- 22 to 171 +/- 16 cmH2O (P < 0.002)], maximum static expiratory pressure [195 +/- 20 to 267 +/- 40 cmH2O (P < 0.002)], and maximum gastric pressure [161 +/- 5 to 212 +/- 40 cmH2O (P < 0.03)]. These parameters were unchanged in the control group. We conclude that nonrespiratory maneuvers can strengthen the inspiratory and expiratory muscles in healthy individuals. Because diaphragm thickness increased with training, the increase in maximal pressures is unlikely due to a learning effect.     

Effect of surface tension of mucosal lining liquid on upper airway mechanics in anesthetized humans.

Upper airway (UA) patency may be influenced by surface tension (gamma) operating within the (UAL). We examined the role of gamma of UAL in the maintenance of UA patency in eight isoflurane-anesthetized supine human subjects breathing via a nasal mask connected to a pneumotachograph attached to a pressure delivery system. We evaluated 1). mask pressure at which the UA closed (Pcrit), 2). UA resistance upstream from the site of UA collapse (RUS), and 3). mask pressure at which the UA reopened (Po). A multiple pressure-transducer catheter was used to identify the site of airway closure (velopharyngeal in all subjects). UAL samples (0.2 microl) were collected, and the gamma of UAL was determined by using the "pull-off force" technique. Studies were performed before and after the intrapharyngeal instillation of 5 ml of exogenous surfactant (Exosurf, Glaxo Smith Kline). The gamma of UAL decreased from 61.9 +/- 4.1 (control) to 50.3 +/- 5.0 mN/m (surfactant; P < 0.02). Changes in Po, RUS, and Po - Pcrit (change = control - surfactant) were positively correlated with changes in gamma (r2 > 0.6; P < 0.02) but not with changes in Pcrit (r2 = 0.4; P > 0.9). In addition, mean peak inspiratory airflow (no flow limitation) significantly increased (P < 0.04) from 0.31 +/- 0.06 (control) to 0.36 +/- 0.06 l/s (surfactant). These findings suggest that gamma of UAL exerts a force on the UA wall that hinders airway opening. Instillation of exogenous surfactant into the UA lowers the gamma of UAL, thus increasing UA patency and augmenting reopening of the collapsed airway.     

Influence of otoliths and neck muscle receptors on peripheral hemodynamic regulation

To evaluate the cardiovascular changes induced by otoliths and neck mechanoreceptors stimulation during head movements, nine subjects in supine prone position performed passive head-down neck flexion (P.Ext) and head up P.Extension (P.Flex) As the lower limbs vasoconstricted from P.Ext to P.Flex, it is suggested that the otoliths stimulation towards the base of the head (like in standing position) contribute to reduce the vasoconstriction whereas when stimulated towards the top of the head (head flexion) they increase it.     

Respiratory function of hyoid muscles and hyoid arch

The position of the hyoid arch suggests that it supports soft tissue surrounding the upper airway (UA) and can act to maintain UA patency. We also suspected that muscles inserting on the hyoid arch might show respiratory patterns of activity that could be affected by respiratory stimuli. To test these possibilities, we moved the hyoid arch ventrally in six anesthetized dogs either by traction on it or by stimulation of hyoid muscles. UA resistance was decreased 73 +/- (SE) 6% and 72 +/- 6% by traction and stimulation during expiration and 57 +/- 15% and 52 +/- 8% during inspiration. Moving averages of the geniohyoid (GH) and thyrohyoid (TH) obtained in six other dogs breathing 100% O2 showed phasic respiratory activity while the sternohyoid (SH) showed phasic respiratory activity in only two of these animals and no activity in four. With progressive hypercapnia, GH and TH increased as did SH when activity was already present. Airway occlusion at end expiration augmented and prolonged inspiratory activity in the hyoid muscles but did not elicit SH activity if not already present. Occlusion at end inspiration suppressed phasic activity in hyoid muscles for as long as in the diaphragm. After vagotomy activity increased and became almost exclusively inspiratory. Activity appeared in SH when not previously present. Duration and amplitude of hyoid muscle activity were increased with negative UA pressure and augmented breaths. We conclude that the hyoid arch and muscles can strongly affect UA flow resistance. Hyoid muscles show responses to chemical, vagal, and negative pressure stimuli similar to other UA muscles.     

Reflex constriction of human limb resistance vessels to head-down neck flexion

The effect of head-down neck flexion on forearm and calf blood flow was determined in 10 healthy male subjects. The subject lay prone, with the neck slightly extended and the chin resting on a soft-padded support at the edge of the table. The chin support was then removed, and the subject maximally flexed and lowered the neck. This was followed by return to the initial position. Neck flexion caused a rapid decrease in blood flow in both forearm and calf; at 30 s this averaged 39 and 35%, respectively. The flow in both forearm and calf gradually recovered as the neck flexion was sustained and approached the control values at the end of 10 min. The blood flow at the ankle was unchanged, indicating that the decrease occurred in the skeletal muscles. The arterial blood pressure and heart rate were unchanged; thus the decrease in flow was due to vasoconstriction. The fact that the decrease was evident as soon as the head was lowered indicated that it was nervously mediated. Neither contraction of the flexor muscles of the neck nor venous congestion of the head, in the absence of the head-down position, altered the blood flow. Although the mechanism of the decrease in flow has not been determined, the studies demonstrate that in response to certain stimuli, the resistance vessels in the skeletal muscles of the forearm and calf undergo a similar nervously mediated vasoconstriction.     

Threshold effects of respiratory muscle work on limb vascular resistance

The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (Q(L)) and utilized the changes in mouth twitch pressure (DeltaP(M)T) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 +/- 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1-3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and Q(L), limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control (P > 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 +/- 12% reduction in P(M)T with bilateral phrenic nerve stimulation. During the fatigue trial, Q(L) and LVR were unchanged from baseline at minute 1, but LVR rose 36% and Q(L) fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and Q(L) returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and Q(L), whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in Q(L). We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions.     

Further evaluation of an EMG technique for assessment of the deep cervical flexor muscles

A novel surface electromyographic (EMG) technique was recently described for the detection of deep cervical flexor muscle activity. Further investigation of this technique is warranted to ensure EMG activity from neighbouring muscles is not markedly influencing the signals recorded. This study compared deep cervical flexor (DCF) muscle activity with the activity of surrounding neck and jaw muscles during various anatomical movements of the neck and jaw in 10 volunteer subjects. DCF EMG activity was recorded with custom electrodes inserted via the nose and fixed by suction to the posterior mucosa of the oropharynx. Surface electrodes were placed over the sternocleidomastoid, anterior scalene, masseter and suprahyoid muscles. Positioned in supine, subjects performed isometric cranio-cervical flexion, cervical flexion, right and left cervical rotation, jaw clench and resisted jaw opening. Across all movements examined, EMG amplitude of the DCF muscles was greatest during neck movements that would require activity of the DCF muscles, particularly during cranio-cervical flexion, their primary anatomical action. The actions of jaw clench and resisted jaw opening demonstrated significantly less DCF EMG activity than the cranio-cervical flexion action (p < 0.05). Across all other movements, the neighbouring neck and jaw muscles demonstrated greatest EMG amplitude during their respective primary anatomical actions, which occurred in the absence of increased EMG amplitude recorded from the DCF muscles. The finding of substantial EMG activity of the DCF muscles only during neck actions that would require their activity, particularly cranio-cervical flexion, and not during actions involving the jaw, provide further assurance that the majority of myoelectric signals detected from the nasopharyngeal electrode are from the DCF muscles.     

Influence of genioglossus tonic activity on upper airway dynamics assessed by phrenic nerve stimulation.

Upper airway (UA) dynamics can be evaluated during wakefulness by using electrical phrenic nerve stimulation (EPNS) applied at end-expiration during exclusive nasal breathing by dissociating twitch flow and phasic activation of UA muscles. This technique can be used to quantify the influence of nonphasic electromyographic (EMG) activity on UA dynamics. UA dynamics was characterized by using EPNS when increasing tonic EMG activity with CO(2) stimulation in six normal awake subjects. Instantaneous flow, esophageal and nasopharyngeal pressures, and genioglossal EMG activity were recorded during EPNS at baseline and during CO(2) ventilatory stimulation. The proportion of twitches presenting an inspiratory-flow limitation pattern decreased from 100% at baseline to 78.7 +/- 21.4% (P = 10(-4)) during CO(2) rebreathing. During CO(2) stimuli, maximal inspiratory twitch flow (VI(max)) of flow-limited twitches significantly rose, with the driving pressure at which flow limitation occurred being more negative. For the group as a whole, the increase in VI(max) and the decrease in pressure were significantly correlated with the rise in end-expiratory EMG activity. UA stability assessed by EPNS is dramatically modified during CO(2) ventilatory stimulation. Changes in tonic genioglossus EMG activity significantly contribute to the improvement in UA stability.     

The effects of neck flexion on cerebral potentials evoked by visual,auditory and somatosensory stimuli and focal brain blood flow in related sensory cortices

Background

A flexed neck posture leads to non-specific activation of the brain. Sensory evoked cerebral potentials and focal brain blood flow have been used to evaluate the activation of the sensory cortex. We investigated the effects of a flexed neck posture on the cerebral potentials evoked by visual, auditory and somatosensory stimuli and focal brain blood flow in the related sensory cortices.

Methods

Twelve healthy young adults received right visual hemi-field, binaural auditory and left median nerve stimuli while sitting with the neck in a resting and flexed (20° flexion) position. Sensory evoked potentials were recorded from the right occipital region, Cz in accordance with the international 10–20 system, and 2 cm posterior from C4, during visual, auditory and somatosensory stimulations. The oxidative-hemoglobin concentration was measured in the respective sensory cortex using near-infrared spectroscopy.

Results

Latencies of the late component of all sensory evoked potentials significantly shortened, and the amplitude of auditory evoked potentials increased when the neck was in a flexed position. Oxidative-hemoglobin concentrations in the left and right visual cortices were higher during visual stimulation in the flexed neck position. The left visual cortex is responsible for receiving the visual information. In addition, oxidative-hemoglobin concentrations in the bilateral auditory cortex during auditory stimulation, and in the right somatosensory cortex during somatosensory stimulation, were higher in the flexed neck position.

Conclusions

Visual, auditory and somatosensory pathways were activated by neck flexion. The sensory cortices were selectively activated, reflecting the modalities in sensory projection to the cerebral cortex and inter-hemispheric connections.