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1 Department of Physiology, Dartmouth Medical School, and 2 Thayer School of Engineering, Dartmouth College, Lebanon, New Hampshire 03756
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We used the global field power (GFP) to estimate the magnitude and timing of activation of the somatosensory cortex by respiratory mechanoreceptor afferents in normal humans in response to brief, negative oral pressure pulses applied at the onset of inspiration. We compared responses before (test) and after insertion of a laryngeal mask airway (LMA) that prevented supraglottal airway receptors from sensing the applied stimulus. Evoked potential responses without supraglottic stimulation were smaller, with delayed or missing features, than those with all receptors stimulated. Supraglottic receptors contribute about one-half of the GFP summed over the 100 ms poststimulus, and subglottal receptors, including those in the larynx, provide a GFP response ~38% above baseline. The most obvious difference between test and LMA responses occurred at 55 ms on average, when the LMA GFP lacked activation features seen in the test condition. We conclude that mechanoreceptors above the larynx are responsible for a major portion of the midlatency afferent information arriving at the somatosensory cortex in response to applied pressure pulses.
respiratory sensation; respiratory afferents; somatosensory cortex; laryngeal mask airway
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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INFORMATION FROM MECHANORECEPTORS activated by oral occlusions or applied pressure pulses arrives at the somatosensory cortex (SSC) within 20-60 ms after the onset of a change in mouth pressure, as indicated by features in the respiratory-related evoked potentials (RREPs) (3, 13, 15). It is not possible from these reports to discriminate the source of mechanoreception responsible for the observed features in the RREPs. It is known that intercostal muscle (4), vagal (14), and phrenic nerve afferents (12, 18) activate the SSC with short latency, and laryngeal afferents evoke brain stem responses in humans (16). However, to the best of our knowledge, the effect of upper airway stimulation on evoked SSC responses in humans has not been shown.
In a companion study (2), we used the global field power (GFP) to describe a new technique for reliable identification of the onset of SSC activation. The GFP approach indicates that, on average, subjects show significant activity in the GFP within 25 ms poststimulus, but the approach does not indicate the origination of that early activity among the possible sources of mechanoreception. Because important sites of mechanoreception lie in the upper airway above the larynx, in the larynx itself, in the sublaryngeal trachea and pulmonary structures, and in the respiratory muscles and the chest wall, the possible sources of afferent activity are broadly distributed throughout the respiratory system. The aim of the research reported here was to quantify and locate in time the contribution of supraglottic airway mechanoreceptor afferent information by comparing the temporal course of GFP activation with and without the insertion of a laryngeal mask airway (LMA), a device that protects supraglottic receptors from stimulation by oral pressure pulses. Our findings indicate that upper airway receptors provide a significant fraction of the GFP activity and that a major portion of that contribution arrives at the SSC at 50-65 ms poststimulus.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Experiments were performed in eight healthy, normal subjects (7 men and
1 woman, age range 20-56 yr) who were paid to be tested on 
1 day
in experiments that involved procedures similar to those described in
our companion study (2). We refer to that companion study for specific
details of the apparatus and procedures, except to note differences and
provide a basic background. As in the companion study, in subjects with
replicate experiments, results were averaged to provide a single value
of each variable measured for each subject.
Electrical measurements. As in the companion study (2), we used a 30-electrode rectangular montage to monitor activity on the right side of the scalp and the underlying SSC: 5 columns anterior-posterior, 6 rows medial-lateral, with the second row sited on and aligned with the nasion-inion midline and centered on the vertex (Cz in the international 10-20 convention). All RREP channels were referenced to the right ear (A2). We also measured the masseter electromyogram (EMG) with a bipolar electrode placed over the muscle judged by voluntary tensing; the electrodes were spaced 4 cm apart.
The electroencephalogram (EEG) and EMG signals were amplified and filtered by a set of 31 low-noise, carefully matched amplifiers, as described previously (2). These signals and mouth pressure were sampled under control of a computerized virtual instrument, as described previously (2). These data were sampled at 2 kHz for 200 ms after mouth pressure fell ~0.2 cmH2O below atmospheric at inspiratory onset. A delay of ~35 ms was required for our balloon valves to apply the pressure pulse stimulus, and we focus our analysis on the 100-ms period poststimulus (judged manually by identifying the point at which the mouth pressure trajectory just began to deviate from the smooth decline of a normal inspiration) so that we can interpret the evoked responses as mainly exogenous in origin. This is appropriate for our interest here, which is to evaluate the nature of afferent information from a specific reception site by using the magnitude and timing of the scalp activity.Protocol.
As described in the companion study (2), experimental runs were
performed using small (10 cmH2O),
brief (200 ms) negative pressure pulses applied to the oral airway in
the standard test condition and in a control condition in which the
vacuum source was not turned on. A third condition was applied here, in
which an LMA was inserted under topical anesthesia of the supraglottic region. The LMA (Gensia, San Diego, CA) is a semirigid plastic tube
curved to approximate the oropharyngeal airway and fitted with an
inflatable bladder at the distal end (1). It was designed to provide
airway access during inhalation anesthesia without passing through the
vocal cords and is inserted to just above the larynx, where the bladder
is inflated to seal the connection to the airway. The rationale for
this experimental design is illustrated in Fig.
1, which shows the location and activation
of respiratory mechanoreceptors in the supraglottic airway, larynx,
pulmonary structures, and muscles and structures comprising the chest
wall. The LMA effectively prevents mechanoreceptors in the airway above the larynx from being stimulated by the applied oral pressure pulse.
Comparison of the evoked responses between the test and LMA conditions
permits evaluation of the contribution of the supraglottic region to
the evoked responses.
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Data analysis. Trial-by-trial results were processed off-line by procedures programmed in MATLAB (MathWorks, Natick, MA), as described elsewhere (2). Band-pass filtering was performed before computation of ensemble averages of all EEG channels and of the masseter EMG and mouth pressure with 95% confidence regions for each signal. The point in time corresponding to stimulus onset was identified from the ensemble average of mouth pressure by visually determining when the signal began to deviate from the smooth ongoing decline in inspiration. We determined in the companion study (2) that significant activity was present in the control state (with no applied pressure pulse). Therefore, we subtracted the control state ensemble-averaged evoked potential for each electrode from those in the test and the LMA states for subsequent analyses except where noted. The GFP was defined by Lehmann and Skrandies (9), and we applied it as described in our companion study (2). The GFP can be considered to be a spatial standard deviation describing the variation of the RREPs over the monitored field as a function of time. We proposed that the GFP provides a measure of activation of the SSC underlying the scalp potential measurements that is relatively insulated from contamination by EMG activity from facial and upper airway muscles that may be activated by negative upper airway pressure stimuli (2).
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Figure 2 shows the ensemble averages of the
RREPs for the 30 channels of the montage for a representative subject
in the test condition. Although confidence intervals were computed,
they are not shown here to maintain legibility. Large RREP components
appear in temporal synchrony with the masseter EMG, suggesting the
possibility of EMG contamination of the RREPs, as discussed at length
in the companion study (2). The RREPs from the same subject after installation of the LMA are shown in Fig.
3, and two points should be made. First,
the evoked response features appear to be smaller and perhaps later
when supraglottic receptors are excluded. This was commonly noted
across subjects. Second, the evoked masseter EMG response in this
subject is greatly reduced after placement of the LMA. This was
uncommon and was not reflected in the mean effect across subjects (see
below). RREP and masseter EMG signals in the control condition were not
significantly different from zero, as judged by computed 95%
confidence regions in most experiments, and the few significant control
RREP responses that were observed were small by comparison to the test
and LMA responses.
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The GFP time course corresponding to the test condition responses of
Fig. 2 after correction for control is shown in Fig. 4A,
together with an estimate of the prestimulus variability. Figure
4B shows the composite plots of all 30 RREP signals from Fig. 2, after subtraction of the control RREPs, that
were used to compute the GFP. The calculated 95% confidence region for
the Cz-A2 ensemble average is plotted as a reference for evaluating when the RREP signals had significant features. The variability shown
here for Cz-A2 was typical of that found for other electrodes. Figure
4B is useful to demonstrate the nature
of the GFP as an estimate of the variability of the field potentials as
a function of time. The RREPs in Fig.
4B do not show significant features at
~75 ms, for example, but they do show wide variability at that time
resulting in a peak in the GFP. Figure
4C shows the ensemble-averaged masseter EMG from Fig. 2 for comparison with the RREPs above. The
temporal correlation was calculated for the EMG and Cz-A2 RREP to be
0.53, a highly significant value for the 200-point sequences
used in the calculation. By contrast, the correlation between the
masseter EMG and the GFP was only 0.10, below the 95% critical
level for the correlation coefficient (0.14 for
n = 200).
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After the LMA was inserted, the RREP (LMA-control) and EMG ensemble
averages and the computed GFP were as shown in Fig.
5. The RREP signals are obviously smaller,
and significant positive peaks in the ranges of ~10 ms and 30-40
ms and the negative peak from 40 to 55 ms are missing, replaced by a
negative peak at ~65-70 ms. The GFP is much reduced (as a
consequence of increased homogeneity across electrodes), as is the
masseter EMG response. The reduction in GFP was found across all
subjects with LMA insertion, but the EMG reduction was not commonly
observed (see below).
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The GFP(t) responses during test and
LMA conditions are shown in Fig. 6 for all
eight subjects. The traces represent the data obtained during single
experiments on all subjects, except those in whom replicate experiments
were performed [subjects AD (4 replicates), JML (2 replicates), and
JNM (2 replicates)], in which
cases the time courses were averaged over the number of replicates. It
is obvious that removal of the supraglottic afferent information results in a substantial decrease in the midlatency GFP in most subjects. The responses of Fig. 6 were then averaged across subjects to
obtain the averaged responses plotted in Fig.
7 showing the 95% confidence regions for
the test and LMA conditions for these subjects. There were two time
spans where the 95% confidence regions for the two conditions did not
overlap, ~55-63 and 67-72 ms, indicative of when
significant information from the upper airway arrived at the SSC in the
test state but not with the LMA installed.
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A simple way to quantify the effect of condition (control, test, and
LMA) on the GFP is to estimate the time integral of the GFP signal by
summing the values from 0 to 100 ms poststimulus. The resulting value
for the test condition of Fig. 4 is 234.3 µV compared with 514.2 µV
computed from the data shown in Fig. 5 for the LMA condition. The
results for this GFP summation as a function of condition for each
subject are shown in Fig. 8 with the
across-subject means and confidence intervals for each condition. The
control responses were not subtracted from the test or LMA responses
here to permit evaluation of the background control activity relative
to the other conditions. It is apparent that application of the
pressure pulse to the entire set of mechanoreceptors results in an
increase in the summed GFP compared with the background control level
that is reduced by insertion of the LMA. Figure 9 shows the result of computing the changes
in the summed GFP and normalizing by a reference condition for the
following differences: test-control (to test the effect of applying the
stimulus to all sites of mechanoreception), LMA-test (to test the
effect of removing the contribution of the supraglottic receptors), and
LMA-control (to evaluate the contribution of the receptors still
stimulated after insertion of the LMA). The mean and 95% confidence
region for each test are plotted and indicate that the GFP is
significantly increased to ~123% of the control level by application
of the pressure pulse to the entire system (Fig. 9,
left). Insertion of the LMA reduces
that increase to about one-half (43%) of the original level
(Fig. 9, right). The GFP that
remains after the LMA is placed is on average 38% greater than the
control level (Fig. 9, middle).
ANOVA indicated that the effect of condition was significant
(P 
0.0001), and none
of the confidence intervals intercepted 
= 0.
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Although the mean GFP responses of Fig. 7 indicate the effect of
supraglottic information on the time course of the GFP, it is possible
that the substantial intersubject amplitude differences might have
influenced this finding. We used the amplitude-insensitive technique
described in our companion study to summarize GFP activation times for
all subjects. Briefly, this technique involved segmenting the time span
into one prestimulus period (20 to 0 ms) and 20 5-ms time bins
from 0 to 100 ms poststimulus. The means and variances of each
poststimulus bin were compared with statistics for the prestimulus
period by use of Dunnett's test, as described elsewhere (2). The data
were summarized by counting the occurrence of significant activity in
each bin from all subjects and adding the counts to produce Fig.
10. This technique does not account for
the magnitude of the GFP in any time bin but only resulted in a count
of "1" if that bin was significantly greater than the prestimulus
reference for each subject and condition. Figure 10 shows the frequency
of occurrence of significant GFP activity for our subject group during
each time bin poststimulus. Similar activation profiles hold for test
and LMA responses corrected for the control response until
time bin 11 (55-60 ms), where the incidence of significant GFP activity becomes considerably less in the
LMA state through time bin 14 (70-75 ms). This divergence of the activation timing is apparent
in the cumulative distribution of activation times shown in Fig.
11, which shows a distinct break point at
time bin 11. The break point as
indicated in Fig. 11 shows where upper airway activity is likely to
arrive at the SSC to contribute to the GFP.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Influence of supraglottal afferents on the GFP. Supraglottic mechanoreceptors are activated by changes in upper airway pressure that also affect mechanoreceptors in other sites in the respiratory system with timing that depends on their location. It is likely that the time required for the oral pressure pulse to propagate to intrathoracic tissue is negligible by comparison with the time required for afferent nerve propagation, so the temporal distribution of afferent information to the SSC from the mass of stimulated mechanoreceptors reflects primarily the distribution of transmission lengths and conduction velocities of the various sets of nerves from mechanoreceptors located in upper airway, laryngeal, pulmonary, and chest wall skeletomuscular tissues. The possibility of afferent information arriving as early as 20 ms poststimulus to the SSC and altering the GFP in our subjects is entirely consistent with the time frame of many of the putative sources for mechanoreception, as we discussed in our companion study (2). It is not possible to differentiate the source of the subsequent features in the evoked responses by timing alone.
Removal of one source of afferent activation by insertion of the LMA does permit us to evaluate definitively the contribution of that site of mechanoreception to the resultant GFP estimate of afferent activity after an applied pressure pulse stimulus. It is apparent from the time courses of the GFP in test and LMA conditions (Fig. 7) that early activity is fairly similar in both states, but significant deviations between them appear between ~55 and 70 ms. There may well be earlier differences: the peaks in the test response at ~30 and 40 ms are greatly diminished in the LMA responses and were nearly significantly different in the average across subjects. The differences after 55 ms found here are striking, however, and show a significant influence of supraglottic receptors on the evoked GFP. The same conclusion is obtained from the distribution of time bins showing significant GFP responses after correction for the control baseline activity (Fig. 11). In a few experiments in which we anesthetized the upper airway to the degree required to insert the LMA but applied the pressure pulse stimuli without the LMA installed, we found only small effects of anesthesia per se on the RREPs and the GFP that did not resemble the effect of the LMA at all. This is consistent with the report by Horner et al. (6) that topical anesthesia of the oropharynx in humans reduced genioglossal EMG responses to pressure pulses to a smaller extent than was the case for nasal and laryngeal anesthesia. They used a much more comprehensive anesthetic protocol than we did here: we were only interested in suppressing the gag reflex sufficiently to install the LMA, so it is not surprising that our approach would have had minimal effect on the evoked responses from more deeply situated receptors. The duration of anesthesia is indicated by the fact that the LMA studies required ~40 min to complete once the LMA was installed, and most subjects felt partial return of sensation by the time they removed the LMA. Use of the LMA provides for virtually complete protection of supraglottic receptors from the applied stimulus for as long as the subject can tolerate the device, whereas any attempt to eliminate upper airway contributions to the afferent signal by complete upper airway anesthesia would be much more difficult, requiring far more anesthesia and much more invasive techniques. We cannot rule out the possibility that some of the effect of LMA placement was due to anesthesia of structures not protected by the LMA (e.g., laryngeal structures) or to the systemic effects of lidocaine absorbed from the mucosa, but this was not apparent from our two subjects who had upper airway anesthesia alone without LMA placement. Because most subjects were able to sense voluntary vocal cord closure when the LMA was installed, we suspect that laryngeal receptors were not completely silenced by topical lidocaine spray. It therefore seems most likely that the effects we found were due to the physical action of the LMA on supraglottic receptors. Another factor that differed slightly between test and LMA conditions was the waveform of the pressure pulse. Although we matched the pulse amplitudes closely, the fall time was always steeper with the LMA installed than in the test condition. We would have expected this more dynamic stimulus to enhance the afferent signal through any rate-sensitive mechanisms that might characterize the subglottal receptor field. We believe it is very unlikely that the observed reduced response was due to the increased rate of fall of the oral pressure. The experimental sequence was fixed, in that the LMA condition always had to follow the test and control conditions because of the unknown duration of airway anesthesia. Thus there is a potential time effect that may have influenced the responses, although our experience with previous RREP experiments involving 600-800 trials did not reveal any time effect on the RREPs over a much longer experimental time. Those experiments were done with a small number of electrodes and cannot provide any information about the effect of timing on GFP responses, however. We do not believe it likely that time is a principally important factor here, however.Influence of supraglottal afferents on the masseter EMG.
Because we cannot claim that the GFP provides complete isolation from
EMG contamination from concurrently activated facial and upper airway
muscles, one possibility that could explain the reduction in GFP with
the LMA is that the EMG signal itself was reduced by protecting
oropharyngeal receptors from stimulation and that reduced EMG artifact
was responsible for the reduced RREPs and GFP. We evaluated that by
comparing the masseter EMG activity as measured by the root-mean-square
value measured over the 100-ms span poststimulus in the test and LMA
conditions and normalizing the responses by the same measure from
control responses in the same day's experiments. The results for each
subject and the mean and median responses are shown in Fig.
12 and indicate that there is no
significant effect of LMA installation on the masseter EMG. Complete
anesthesia of the upper airway somewhat reduces but does not eliminate
the genioglossal response to negative pressure pulses applied to the
entire airway (6), although tracheotomized, laryngectomized patients
did not show a genioglossal response when that stimulus was applied to
the tracheostomy (7). As the latter group (7) speculated, receptors
important for the genioglossal response may lie close to and have been
removed with the larynx. The masseter shares other reflex activation
characteristics with the genioglossus (5), so it is not surprising that
the masseter response to negative pressure pulses remains after LMA insertion, which permits stimulation of laryngeal receptors.
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Characteristics of afferents excluded by the LMA. The LMA excluded regions of the upper airway with mechanoreceptors served by the superior laryngeal nerve, the hypoglossal nerve, the glossopharyngeal nerve, the facial nerve, the vagus, and others. Laryngeal mechanoreceptors were still accessible to the stimulus with the LMA installed, and their contribution likely remains in the LMA responses, since the effect of anesthesia alone was minimal. Although it might be tempting to assume that supraglottic afferent information would arrive earliest in the evoked responses because of the proximity of this area to the brain, such is apparently not the case. Onset of SSC activation as indicated by the GFP occurred in some subjects as early as 20 ms poststimulus in this study and in the results of our companion study (2) with or without the LMA (Figs. 10 and 11), well before the major effect attributable to the supraglottic receptors indicated here. This must be due to the slower relative conduction velocities of nerves serving the upper airway than those serving more distant regions of mechanoreception, such as chest wall muscle spindles. Gandevia and Macefield (4) concluded that the ~20-ms latency they measured for intercostal muscle afferents stimulated electrically was consistent with the activity being carried by group II afferent nerves, having a conduction velocity of 35-75 m/s. In contrast, the conduction velocity of the vagus in normal humans was estimated to be 10 m/s by Tougas et al. (14) in response to electrical stimulation.
The roles of receptors excluded by the LMA are not well characterized and are undoubtedly multifaceted. Facial, vagal, and laryngeal afferent projections to the SSC and motor cortical areas in primates have been demonstrated (10), humans show evoked brain stem responses to vibratory stimuli of the superior laryngeal nerve (16), and the upper airway has been shown to participate importantly in load detection in normal humans (11, 17). Horner et al. (6) showed that human genioglossal EMG reflex responses to upper airway negative pressure pulses were reduced when supraglottic receptors were deeply anesthetized. The effect of the LMA to reduce the GFP demonstrated here shows that sensory information reaching the SSC is reduced and suggests that a functional deficit in one or more of these aspects would occur with LMA installation.Control state responses. The presence of small but significant GFP activity in the control state was noted here and is similar to the results we obtained from another set of responses in the companion study (2). Although three of the subjects in this investigation were common to the subject pool for the previous report, none of the data from the previous analysis were included in this report. Thus there appears to be an effect on the GFP due to ongoing inspiration causing mechanoreceptor afferent activity that is, in turn, synchronized to the application of the pressure pulse stimulus near inspiratory onset. Although the control state RREPs showed small activity, correction for this activity emphasized the difference in activation time between the test and LMA conditions. If one is only interested in the effect of a specific maneuver, we recommend always subtracting the control responses from the tested condition. Here, we were interested in the effect of the LMA and the responses in control and test conditions and treated our data as presented.
In summary, we have shown here that supraglottic receptors make a significant contribution to the evoked responses to brief, negative pressure pulses applied to the upper airway. The magnitude of evoked activity as estimated by the summed GFP over 100 ms poststimulus is significantly reduced, primarily by the loss of information arriving at the SSC between 55 and 75 ms. Activation of the masseter muscle in response to these stimuli was not significantly altered. The role of this supraglottal information in respiratory sensation and control remains to be further elucidated, but the fact that the upper airway contribution can be localized in time as indicated provides us with an extremely useful tool to evaluate variation in the GFP in subjects with known upper airway problems. It will be very interesting to determine, for example, how GFP information from patients with obstructive sleep apnea (OSA) compares with that from normal subjects. A decrease in the GFP in the 50- to 65-ms range in patients with OSA would support a hypothesis for the mechanism of OSA related to a defect in afferent traffic from those patients.| |
ACKNOWLEDGEMENTS |
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We thank Robert Hamlin for excellent technical assistance and Lisa M. Lim for contributing to the early development of the project.
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FOOTNOTES |
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This research was supported in part by National Heart, Lung, and Blood Institute Grant HL-29068 and by Whitaker Foundation Grant WF 97-0530.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: J. A. Daubenspeck, Physiology Dept., Borwell Research Bldg., Dartmouth Medical School, Lebanon, NH 03756 (E-mail: andrew.daubenspeck{at}dartmouth.edu).
Received 19 August 1999; accepted in final form 4 November 1999.
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TOP
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METHODS
RESULTS
DISCUSSION
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  D. E. O'Donnell, R. B. Banzett, V. Carrieri-Kohlman, R. Casaburi, P. W. Davenport, S. C. Gandevia, A. F. Gelb, D. A. Mahler, and K. A. Webb Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease: A Roundtable Proceedings of the ATS, May 1, 2007; 4(2): 145 - 168. [Abstract] [Full Text] [PDF]
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 P. W. Davenport, A. D. Martin, Y-L. Chou, and S. Alexander-Miller Respiratory-related evoked potential elicited in tracheostomised lung transplant patients. Eur. Respir. J., August 1, 2006; 28(2): 391 - 396. [Abstract] [Full Text] [PDF]
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S. Redolfi, M. Raux, C. Donzel-Raynaud, C. Morelot-Panzini, M. Zelter, J-P. Derenne, T. Similowski, and C. Straus Effects of upper airway anaesthesia on respiratory-related evoked potentials in humans Eur. Respir. J., December 1, 2005; 26(6): 1097 - 1103. [Abstract] [Full Text] [PDF]
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 C. Donzel-Raynaud, C. Straus, M. Bezzi, S. Redolfi, M. Raux, M. Zelter, J.-P. Derenne, and T. Similowski Upper airway afferents are sufficient to evoke the early components of respiratory-related cortical potentials in humans J Appl Physiol, November 1, 2004; 97(5): 1874 - 1879. [Abstract] [Full Text] [PDF]
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M. Bezzi, C. Donzel-Raynaud, C. Straus, C. Tantucci, M. Zelter, J-P. Derenne, and T. Similowski Unaltered respiratory-related evoked potentials after acute diaphragm dysfunction in humans Eur. Respir. J., October 1, 2003; 22(4): 625 - 630. [Abstract] [Full Text] [PDF]
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M. Akay, J. C. Leiter, and J. A. Daubenspeck Reduced respiratory-related evoked activity in subjects with obstructive sleep apnea syndrome J Appl Physiol, February 1, 2003; 94(2): 429 - 438. [Abstract] [Full Text] [PDF]
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P. W. Davenport and A. A. Hutchison Cerebral cortical respiratory-related evoked potentials elicited by inspiratory occlusion in lambs J Appl Physiol, July 1, 2002; 93(1): 31 - 36. [Abstract] [Full Text] [PDF]
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J. A. Daubenspeck, H. L. Manning, and J. C. Baird Midlatency respiratory-related somatosensory activity and perception of oral pressure pulses in normal humans J Appl Physiol, June 1, 2001; 90(6): 2048 - 2056. [Abstract] [Full Text] [PDF]
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J. A. Daubenspeck, L. M. Lim, and M. Akay Global field power helps separate respiratory-related evoked potentials from EMG contamination J Appl Physiol, January 1, 2000; 88(1): 282 - 290. [Abstract] [Full Text] [PDF]
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