A direct relationship exists within subjects between midlatency features (<100 ms poststimulus) of respiratory-related evoked potentials and the perceived magnitude of applied oral pressure pulse stimuli. We evaluated perception in 18 normal subjects using cross-modality matching of applied pressure pulses via grip force and estimated mechanoafferent activity in these subjects by computing the global field power (GFP) from respiratory-related evoked potentials recorded over the right side of the scalp. We compared across subjects1) the predicted magnitude production for a standard pressure pulse and 2) the slope (β) and 3) the intercept (INT) of the Stevens power law to the summed GFP over 20–100 ms poststimulus. Both the magnitude production for a standard pressure pulse and the β showed an inverse relationship with the summed GFP over 20–100 ms poststimulus, although there was no relationship between INT and the summed GFP. This may partially reflect characteristics of the mechanosensors and surely includes aspects of cognitive judgment, because we found and corrected for a high correlation between, respectively, β (and INT) for pressure pulses and β (and INT) for estimation of line lengths, a nonrespiratory modality. The relatively shallow, even inverse GFP-to-perception relationship suggests that, despite marked differences in the magnitude of afferent traffic, normal subjects seem to perceive things similarly.
- evoked potentials
- global field power
- respiratory mechanoreceptors
that physiological stimulation of the human respiratory system could produce evoked responses measured on the scalp was first presented in 1986 by Davenport's group (7), who showed that inspiratory occlusions were effective in evoking demonstrable midlatency (<100 ms poststimulus) activity in normal human subjects. Other work has shown that afferents from the diaphragm and intercostal muscles project to the somatosensory cortex in cats and humans (8, 10), and it is reasonable to expect that physiological stimulation should produce respiratory-related evoked potentials (RREPs) with midlatency components reflective of the nature of afferent activation of the entire set of respiratory mechanoreceptors distributed throughout the respiratory system. Our laboratory has explored the character of the RREPs evoked by small, brief, negative pressure pulses applied at the onset of inspiration (4, 6, 15, 18) and has been able to separate reliably much of the contamination caused by concurrent activation of muscles of the face and upper airway. These muscles respond reflexively to the negative-pressure airway stimulus, and, by computing the global field power (GFP), we obtain an indication of the variation of evoked activity over the monitored electrode set (4). The GFP is a reference-independent measure of evoked activity that reflects activation of the underlying cortex (14). By focusing on the nature of the evoked responses within 100 ms poststimulus, we have a reliable index of the time course and magnitude of the afferent information from respiratory mechanoreceptors produced by the applied pressure-pulse stimulus.
Perception of respiratory mechanical stimuli depends on cognitive processing of afferent information from peripheral mechanoreceptors and can involve determination of the threshold value of a stimulus required for detection or estimation of magnitudes over a range of stimuli above the detection threshold. Signal detection may only require activation of the most sensitive of a set of parallel sensory pathways, but it is likely that magnitude estimation involves evaluation of information from multiple receptor pathways. Stevens' power law is commonly used to describe magnitude estimates as a function of stimulus intensity. That is Equation 1where Ψ is the perceived magnitude, K is a constant, Φ is the stimulus intensity, and β is Stevens' exponent. This relationship is conveniently evaluated by taking the log of both sides to obtain a relationship linear in log-log coordinates for which the slope is β [i.e., log(Ψ) = log(K) + β log(Φ)].
Integration of afferent information to form a magnitude estimate should depend on the character of the afferent signals available for cognitive processing in the cortex. It has been shown that, in a given subject, a direct relationship exists between the amplitude of midlatency evoked potentials and the Ψ of the applied stimulus for tactile (9) and respiratory (11, 12) modes of sensation. This suggests that the features of the measured scalp-evoked activity are closely correlated with the afferent neural signal serving as the input to cognitive processing. In our experience with RREPs occurring in response to oral pressure pulses, we have seen a wide range in the magnitudes of the evoked responses across our sample of normal human subjects (4, 6), and we wondered if this would result in a similarly wide range of magnitude estimation characteristics. To our knowledge, there has been no previous comparison for any modality of perception and cortical evoked activity across subjects, although one report has described the relationship between afferent activity in peripheral nerves and perception of the evoking mechanical stimulation of receptors in the hand of human subjects (13).
We hypothesized that subjects who showed a greater amount of afferent activation as indicated by a large GFP signal in the time from the earliest appearance of afferent activity (∼20 ms after oral pressure pulse onset through 100 ms poststimulus) would show greater perception of the applied pressure. Because we have found more intersubject variation in subjects' responses to applied stimuli than to the control activity observed when no stimulus is applied, we expected subjects with greater evoked activity to demonstrate greater sensitivity to the stimulus as evidenced by a larger estimated magnitude for a standard applied pressure pulse. The rationale for this hypothesis is simply that subjects with a greater amount of afferent activity to an applied stimulus would likely translate that increased afferent traffic into a larger perceptual estimate. The focus of this study concerns the way in which variation among subjects in the GFP (the afferent signal) explains variation in intersubject perception. Preliminary results have been reported previously based on a smaller data set (5).
Results are reported here from experiments performed on 18 normal subjects for whom pressure pulse perception and evoked response data sets were obtained. The subjects were all volunteers who were paid to participate in the study. Informed consent was obtained for protocols approved by our local Institutional Review Board. Subjects ranged in age from 18 to 57 yr [mean 31.9 ± 11.9 (SD) yr; median 30 yr]; there were 11 men and 7 women. Some aspects of the GFP responses have been reported (4, 6); the perception data have not previously been reported.
Our laboratory has elsewhere described in detail the techniques we use to measure evoked responses (4, 6) and will only briefly summarize them here. Earlier experiments tested 12 subjects wearing a 30-electrode rectilinear montage (5 columns of electrodes in the anterior-posterior direction, 6 rows in the medial-lateral direction) mounted on a stretchable cap (Electro-Cap International, Eaton, OH) sited on the right side of the scalp overlying the expected location of the somatosensory cortex. Later experiments on six subjects involved a bilateral array of 60 electrodes covering the somatosensory area on both sides of the scalp, but only results based on the right-side electrodes will be reported here to permit inclusion of earlier and later subjects in a single consistent database. The areas monitored and electrode spacing were very similar for both data sets. Electrode impedances of <5 KΩ were achieved, and, when noise on an electrode indicated that impedance had changed, the electrode gel was gently adjusted to refresh the signal quality. We used 30 or 60 closely matched, high-impedance (>2 GΩ) isolated amplifiers (EPA6, Sensorium, Charlotte, VT) with gains of 40K and band-pass filters between 0.1 and 500 Hz to amplify the scalp signals.
Subjects breathed on an apparatus designed to permit brief (200-ms) negative pressure pulses to be applied at inspiratory onset by a computer-controlled apparatus located outside the room in which the subject sat in a comfortable dental chair within a large Faraday cage. Pressure-pulse amplitudes of −5 to −30 cmH2O relative to atmospheric pressure were generated by a variable vacuum source. For the evoked responses, a standard −10-cmH2O pulse was used; the magnitude estimation tests applied pressures over the full range of −5 through −30 cmH2O.
Subjects generally performed the magnitude estimation task first and returned on a later day to perform the evoked potential experiment, although occasionally these experiments were performed on the same day. Perception was evaluated by using a cross-modality technique patterned after that described by Muza and Zechman (16) using a handgrip dynamometer with electrical output. Magnitude estimation of pressure pulses was accompanied by a line-length estimation task to evaluate how individual subjects used the handgrip force transducer with a nonrespiratory perception task. Horizontal bars of six different lengths were projected on the wall of the darkened experimental room. Six sequences of the six lengths (randomized order) were presented. Subjects were given standardized instructions to match their grip force to the length of the projected line and, when they had achieved the appropriate force, to press a button to indicate that their choice was valid. The grip-force and button data were recorded on an on-line computer running an electronic strip-chart program (CODAS, DataQ, Cleveland, OH) for later analysis.
After the line-length test, subjects were given a series of thirty-six 200-ms pressure pulses at six levels, from −5 through −30 cmH2O, randomized within six replicate sequences. The pressure-pulse magnitude was modulated by using a variable transformer to vary the vacuum source; the replicated stimuli were close to, but not exactly identical to, the target for each pressure level. A light-emitting diode lit during expiration alerted subjects that a pressure pulse would accompany the next inspiration, and they were instructed to match their grip force to the perceived size of the pressure pulse and to press the button when their evaluation was satisfactory. The same electronic strip chart used for line-length tests was used to record the pressure amplitude, grip force, and button signal. A pressure pulse resulting in airway collapse was immediately apparent in the oscillation of mouth pressure. Such a trial was marked as defective and repeated.
After perception tests were complete, evoked potential measurements were obtained in different experiments for sets of ∼100 trials with −10-cmH2O pressure pulses. When inspiratory pressure exceeded −0.2 cmH2O, the pressure pulses were applied by an on-line computer data-acquisition and control program (LabVIEW, National Instruments, Austin, TX). This system monitored mouth pressure, activated a set of computer-controlled balloon valves to apply the pressure pulse, and digitized 200-ms sequences of 30 or 60 electroencephalogram (EEG) channels and mouth pressure at 2 kHz. All 30 or 60 EEG channel samples plus mouth pressure were displayed on a dual-monitor system running on a laboratory computer (Macintosh G3, Apple, Cupertino, CA) for quality evaluation before being saved to disk. Only trials in which the EEG was uncontaminated by eye movements or other artifact, and for which the pressure pulse was of the correct amplitude and uncontaminated by airway collapse, were saved to disk for later analyses. Each experiment included a control set of 100 trials performed under conditions identical to the test conditions but with the vacuum source turned off.
The line-length experiments were analyzed by measuring the grip force exerted in response to each projected line length and by fitting a linear regression line to the log-log plot of grip force as a function of line length. The first sequence of six line lengths, the training set, was discarded for each subject. The slope of this log-log regression was interpreted as the β and the antilog of the intercept as the K. We noted that, in virtually every subject, the grip force for the longest of the six lines lay consistently above the regression line that was a reasonable fit to the other five line-length results, and it was apparent that subjects were induced to squeeze harder when they noted that the line filled the screen onto which it was projected. We, therefore, omitted the longest line length from all analyses, leaving 25 line-length trials to comprise the response data set. If the subject responses resulted in a fitted line that was visually adequate and had a correlation coefficient of ≥0.5, the result was retained for further analysis. Acceptable line-length data were obtained from 13 of the 18 subjects, and the median correlation coefficient for the regressions included was 0.82. Replicate tests were performed in a few subjects, and their results were averaged over the number of their adequate trials to provide a single estimate.
The pressure pulse perception experiments were analyzed in an analogous manner. The first sequence of pressure pulses (the training sequence) was omitted from analysis, and the slope of the fitted regression line to the remaining 30 pressure applications gave the β for perception of oral pressure pulses. Adequate responses were estimated in all 18 subjects, with the median correlation coefficient for the regression being 0.79. For the few subjects in whom replicate experiments were performed, replicate values for K and β were averaged to obtain representative values for each subject. From the fitted values for K and β for each subject, we calculated the expected magnitude estimate for a 10-cmH2O pressure pulse (ME10). This value was used as a functional estimate of perception that includes both slope and intercept information.
Evoked response analysis.
Off-line analyses included trial-by-trial band-pass filtering (10–160 Hz) and ensemble averaging of the 30 channels of EEG. Filtering was performed by using routines programmed in a general-purpose analysis package (MATLAB, Mathworks, Natick, MA) and was designed to filter each trial twice, once forward and then backward, to eliminate any phase shift due to filtering. Ensemble averaging was also performed by routines programmed in MATLAB, and these routines returned the mean respiratory-related evoked responses with 95% confidence intervals to evaluate the reliability of the response from each channel.
The GFP is computed by Equation 2adapted from Ref. 14, where theui (tk ) anduj (tk ) are the RREP signals at each electrode at the time tk taken in all possible pairs, measured relative to a common reference (here the right ear, A2), and n is the number of electrode positions used. The difference between ui anduj at time tk is independent of the reference electrode used, and the GFP is, therefore, a reference-independent measure of the evoked activity. The GFP is a measure of the spatial variation of the potentials at each point in time over an electrode field and, as described in Eq. 2 , represents a spatial standard deviation. It was computed for the set of electrodes measured in each experiment, nominally 30, although, in a few experiments, excessive noise, identified as large-amplitude signals with large confidence regions, required the omission of one to three channels from the computations. As described previously (4,6), we subtracted the ensemble-averaged RREP signals obtained during control experiments (no pressure applied) from the RREP in the test condition with the −10-cmH2O stimulus before computing the GFP.
The stimulus onset time was identified from plots of the mouth pressure vs. time as the point at which the inspiratory pressure trajectory deviated from the smooth decline of the ongoing inspiration. As our laboratory described previously (6), the summation of the GFP(t) over a time period provides a useful index of afferent activity over any particular period between stimulus onset and 100 ms poststimulus. Here we computed the summed GFP over the periods 20–100 ms (GFP20–100) and 50–80 ms (GFP50–80) poststimulus to estimate respiratory mechanoreceptor input to the cognitive processes that result in perceptual evaluation of the stimuli.
Perception data and fitted lines on log-log plots are shown in Fig. 1 for line-length and pressure pulse responses from a subject with a high β for pressure pulse stimuli (βPP). The pressure pulse responses in Fig. 1 Awere best fitted on the log-log plot by a line with a slope of 1.08 and intercept of −1.87 with a correlation coefficient of 0.88. The line-length responses for the same subject are shown in Fig.1 B and were best fitted by a log-log slope of 1.16 with an intercept of −1.32 and a correlation coefficient of 0.89. Figure2 shows analogous pressure pulse (Fig.2 A) and line-length (Fig. 2 B) magnitude estimation responses for a subject with a low βPP. Pressure pulse estimates were best fitted with a log-log slope of 0.34 with an intercept of −0.62 and a correlation of 0.74, whereas the line-length estimates were best characterized by a slope of 0.69, an intercept of −0.55, and a correlation of 0.81. The pressure pulse responses for the 18 subjects yielded an average slope of 0.70 ± 0.07 (SE). Line-length responses from the 13 subjects with acceptable line-length data yielded a mean slope of 0.91 ± 0.08.
The predicted ME10, based on each subject's individual estimated β and intercept are shown in Fig. 3 and are plotted as a function of the individual values for the GFP20–100. The plot shows the predicted magnitude vs. the log of the GFP20–100 as that transformation produced a reasonably linear relationship and a significant regression; the plot vs. the untransformed data seemed to be best fit by a hyperbolic-like function and did not produce a significant linear relationship. We do not now have a theoretical basis for why the logarithmic transformation adequately captures a linear data trend.
The relationship of the predicted magnitude estimates with the estimates of afferent activity shown in Fig. 3 is not consistent with our original hypothesis, and this will be discussed later. We examined the extent to which the relationship between the predicted perception and the afferent signal was affected by the separate contributions of the slopes and the intercepts of the fitted perception responses, and Figs. 4 and5 show the relationships between each aspect of the perception response (slope, Fig. 4, and intercept, Fig.5) vs. the GFP20–100. A highly significant, inverse relationship holds between the β (Fig. 4) and the afferent signal, but there is no apparent relationship between the intercept and each subject's afferent activity (Fig. 5).
The most important finding of this study is that subjects who appear to have greater afferent information from respiratory mechanoreceptors do not necessarily perceive a standard pressure pulse stimulus to have a greater magnitude, compared with subjects seeming to have less afferent traffic. This contradicts our original hypothesis that there would be a direct relationship between afferent traffic and perception. The conclusion that, across subjects, an inverse relationship exists between afferent traffic and perception is dependent on a number of assumptions, which we discuss below.
We have interpreted the GFP20–100 as an estimate of afferent activity from respiratory mechanoreceptors over that period. This assumes that somatosensory activity over that period is relatively uncontaminated by endogenous processing of the afferent activity. Such an assumption is clearly not tenable in detail, based on the long-standing knowledge that sleep affects components of similar latency in median nerve somatosensory evoked responses (1, 17,21). More pertinent to RREPs, sleep has been shown to affect components in the evoked responses with latencies >100 ms postocclusion, but sleep effects were much less apparent with regard to shorter latency components (19). Similarly, a recent report by Webster and Colrain (20) on the effects of attention on mid- and longer latency components of the evoked response to occlusion pressure stimuli showed that the only effect of attention on components with latencies within the time period of interest to us was to delay the P1 component from 54 to 67 ms; there was no effect of attention on the amplitudes of any components with latencies <100 ms. In a previous report (18) looking at evoked responses to pressure pulses in attending and nonattending conditions, our laboratory did not see any effect on the evoked responses that occurred <100 ms poststimulus. It is likely that subtle modulation of some aspects of RREPs occurs within the 100-ms poststimulus span of interest, but that does not preclude the use of that information to examine exogenous evoked activity, provided the state of arousal is reasonably consistent within and between experiments (as was the case here). Therefore, we feel that our interpretation of the GFP20–100 as an index of afferent activity is reasonable, especially as it is less contaminated by electromyographic activity from concurrently activated facial and upper airway muscles than are direct measures of evoked responses (4).
Our data (Fig. 3) indicate that the relationship between perception and afferent activity, as captured in the relationship between the predicted estimate to a standard −10-cmH2O pressure pulse stimulus and the GFP20–100, is opposite to what we hypothesized. Subjects with greater GFP activity to −10-cmH2O pressure pulses had smaller predicted magnitude estimates to that pressure stimulus. Rather than conversion of afferent activity into Ψ in a direct relationship as we had expected, it appears that subjects receiving greater afferent information attenuate their perception of the causative stimulus. There was also an inverse relationship between the βPP and the summed GFP (Fig. 4), but there was no apparent relationship between the power law intercept and the amount of afferent traffic as estimated by the GFP.
There are at least two complicating issues that need to be considered with regard to the measurements. The first is whether the magnitude estimation parameters for pressure pulse stimuli are valid. This is not an easy question to answer because, to our knowledge, there are no published data regarding the perception of this stimulus. Muza and Zechman (16) reported a β for peak mouth pressure of 1.22, measured during loaded breathing, and we can compare our β for the peak applied pressure pulse to that value if we correct our value for the grip force exponent of 1.7 (16). Thus, if we multiply our average βPP of 0.70 by 1.7, we obtain a value of 1.20, quite close to the result of Muza and Zechman. We, therefore, feel that our magnitude estimates are reasonable.
The second issue is whether our GFP results could be systematically affected by volume conductivity differences among subjects that might create an inverse relationship between scalp estimates of afferent activity and magnitude estimates that otherwise might actually follow our hypothesis. For example, what if the subjects with high measured GFP values had a lower value for skull resistance, the major resistive component between the cortical sites of sensory activity and the scalp where activity is measured? If this were true, for any given level of local cortical activation, subjects with lower skull resistance would have greater local radial currents through the skull, and this would increase the local variation in scalp potentials and augment the GFP. To compensate for this, we would have to correct the high-GFP measurements downward and the low-GFP measurements upward. Such a correction would only serve to steepen the inverse slope for the relationship of ME10 or βPP vs. GFP and could only produce the hypothesized direct relationship between perception and afferent activity if the corrections were large enough to actually reverse the sign of the slope. We think that this is very unlikely because it would require subjects with high GFP measured on the scalp to have less cortical activity than subjects with low scalp GFP values.
What could explain the inverse relationship between sensation and perception observed among subjects? The conversion of an afferent stimulus into a perception involves a sensory and a cognitive aspect, and the observed response could have its explanation in either or both of these. One of us has proposed a model for the sensory afferent process (2, 3), the sensory aggregate model (SAM), which describes the expected response of a population of sensory afferents with different activation thresholds. Figure6 demonstrates the expected afferent responses from two subjects having afferent mechanoreceptor populations that consist of the same number of receptors, each with identical stimulus-response shapes (logistic) and mean values for their activation thresholds but that differ only in the variance of the distribution of activation thresholds. Figure 6 shows the population responses to identical applied (fixed) stimuli at any level below some maximum. We assume that the afferent activity arriving at the somatosensory cortex is proportional to the summation of receptor activity from all receptors whose activation threshold lies at or below the level of the applied pressure stimulus. Clearly, the summed afferent activity (GFP) will be greater for the more broadly distributed population (left) than for the more narrow distribution (right). This corresponds to the response for the −10-cmH2O applied pressure pulse. In Fig.7, we illustrate the effect of this difference in the distribution of activation thresholds on perception as measured by magnitude estimation. We hypothetically apply a series of stimuli over a range of magnitudes and assume that the slope of the magnitude estimate will reflect how much the afferent activity changes with an increase (or decrease) in applied stimulus magnitude. Because the population on the right is more narrowly distributed, the full range of afferent activity will be encompassed by a smaller range of applied pressures than will be true for the more broadly distributed population on the left. Thus the more narrowly distributed activation threshold population would lead to a steeper slope between applied pressure and magnitude estimates. This analysis shows that the SAM model is consistent with our observation that subjects with higher GFP tend to produce a lower estimate of a standard pressure pulse stimulus (Fig. 3) and a lower exponent (Fig. 4).
However, this consistency does not mandate acceptance of the SAM model as the explanation for our observations. On the basis of our results, it is likely that subjects do differ with respect to the afferent activity that they receive from their respiratory mechanoafferents, because we cannot think of a reasonable alternative to explain why they differ so in their GFP responses to a −10-cmH2O stimulus. If we omit the two smallest and two largest GFP responses to minimize the effect of outliers, we still find nearly an order of magnitude difference between the remaining highest and lowest GFP responses to the standard −10-cmH2O stimulus. With respect to the cognitive processing of that afferent information, however, subjects may yet modulate their magnitude estimation based on learned experiences and other cognitive factors. We measured subjects' magnitude estimation characteristics with respect to both a respiratory task and a nonrespiratory task (evaluation of line lengths). Figure8 (which compares the individual β values for these two modalities, which process completely different sensory inputs) and Fig. 9 (which compares the fitted intercepts) indicate surprising and significant correlations between the power law parameters for these two quite distinct sensory modalities. Subjects with a higher β for line length (βLL) also have a higher βPP (and likewise for intercepts), suggesting that some aspect of the judgment process consequent to sensory afferent processing determines a portion of the magnitude estimation, regardless of the sensory modality. Over the ranges of pressure pulse and line-length stimuli tested, the ratio of the highest to lowest βLL was ∼3.3, and the ratio for βPP was ∼3.0, indicating a similar range of judgment effects for both modalities. Considering the power law intercept variation, the ratio of maximum to minimum for line length was ∼5.4, whereas the ratio for pressure pulse stimuli was nearly 7.0. There was no significant relationship between the exponent and intercept within either stimulus modality.
We used the regression results for βPP regressed on βLL from Fig. 8 and for the intercept results from Fig. 9to correct each subject's βPP and intercept for perception of pressure pulses (INTPP) for the individual tendency of each subject to over- or underexpress his or her perception using the force-grip cross-modality approach. This correction reduced each subject's pressure pulse slope and INTPP by an amount computed using the regression results of the pressure pulse slope and INTPP from all 13 subjects for whom both pressure pulse and line-length data were available, together with each of the 13 subjects' line-length slope and intercept. The corrected β and corrected intercept for each subject were used to compute a corrected estimate of the ME10 stimulus that accounts for each subject's individual characteristics using the cross-modality expression of line length. The corrected ME10 is plotted vs. the GFP20–100 in Fig.10, together with the best fit regression line. The resulting regression is significant (P < 0.01), and the inverse relationship is still apparent. The cognitive component related to using grip force to express perception of respiratory pressure pulses adds variability to the relationship between the β and the afferent signal, and accounting for the nonrespiratory variation in magnitude estimation in this manner reduces the range of variation in the ME10 responses from a maximum-to-minimum ratio of 3.29 to 1.82. A significant effect of afferent magnitude remains, and this may be attributable to the SAM explanation offered earlier or have other cognitive sources.
Our laboratory has previously shown that information from upper airway mechanoreceptor afferents arrives in normal subjects roughly between 50–80 ms poststimulus (6), and we wondered how well information from that time span correlated with the corrected estimates of perception of the −10-cmH2O pressure pulse stimulus. Figure 11 shows this relationship and indicates that a virtually identical relationship holds for both the 20- to 100-ms and the 50- to 80-ms summations of afferent activity. It is reasonable to speculate, therefore, that supralaryngeal mechanoreceptor activity may largely contribute to the perception of pressure pulse stimuli in our subjects.
The net effect of the relatively shallow, inverse relation between afferent activity and perceptual sensitivity is that subjects will tend to return magnitude estimates that are much more similar across the subject population than would be the case if our hypothesized direct relationship pertained with steep slope. The shallow relationship that we found between perception and somatosensory activation by respiratory stimuli is similar to the lack of correlation reported by Knibestöl and Vallbo (13) between perception and afferent nerve responses to mechanical stimulation of receptors in the hand, although our finding of the small but significant negative relationship is unexplained. It is possible that humans adapt to the amount of afferent information provided by their individual mechanoreceptor characteristics. It might be quite distracting for those with highly sensitive mechanosensation to be as responsive as those with less-sensitive sensory mechanisms to ongoing mechanical information consequent to breathing. Therefore, the shallow, inverse relation between perception and afferent activity may result from hereditary or adaptive variation in cognition that serves to modulate the impact of natural stimuli on brain function.
We thank Robert Hamlin for excellent technical assistance. We also thank Dr. Abraham Guz for thoughtful advice.
This research was supported by National Heart, Lung, and Blood Institute Grant HL-29068.
Address for reprint requests and other correspondence: J. A. Daubenspeck, Physiology Dept., Borwell Research Bldg., Dartmouth Medical School, Lebanon, NH 03756 (E-mail:).
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. Section 1734 solely to indicate this fact.
- Copyright © 2001 the American Physiological Society