accuracy of symptom perception in asthma and illness severity

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Accuracy of SymptomPerception in Asthma andIllness SeveritySimon Rietveld , Pier J. M. Prins & Vivian T. CollandPublished online: 07 Jun 2010.

To cite this article: Simon Rietveld , Pier J. M. Prins & Vivian T. Colland (2001)Accuracy of Symptom Perception in Asthma and Illness Severity, Children's HealthCare, 30:1, 27-41, DOI: 10.1207/S15326888CHC3001_3

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Accuracy of Symptom Perception inAsthma and Illness Severity

Simon Rietveld and Pier J. M. PrinsDepartment of PsychologyUniversity of Amsterdam

Vivian T. CollandHeideheuvel Asthma CenterHilversum, The Netherlands

The inaccurate perception of airway obstruction is a risk factor in fatal asthma and acommon problem in asthma management. Perceptual inaccuracy often has been at-tributed to airway pathophysiology. Accuracy is defined in terms of airway obstruc-tion, reflected in lung function. The accuracy of symptom perception was investi-gated during induced airway obstruction. In Experiment 1, 30 children andadolescents with asthma underwent a histamine provocation test. In Experiment 2, 64children and adolescents with asthma and 30 without asthma performed a physical ex-ercise task. Ages ranged from 7 to 18 years. Lung function and self-reported dyspneawere measured in parallel. The results showed that dyspnea reporting was independ-ent of lung function (Forced Expiratory Volume in 1 sec), asthma severity, and airwayhyperresponsiveness. Participants with asthma but without airway obstruction re-ported significantly more dyspnea than controls. It was suggested that dyspnea is ahighly subjective experience with its magnitude determined by psychological and sit-uational factors rather than airway pathophysiology.

Childhood asthma is a chronic respiratory disorder characterized by recurrent epi-sodes of airway obstruction and dyspnea (breathlessness). The relation betweenairway obstruction, expressed in lung function parameters, and dyspnea magnitudereflects the accuracy of symptom perception.

Inaccurate symptom perception is a common problem in asthma managementand a risk factor in fatal asthma (Barnes, 1994). The early perception of airway ob-

CHILDREN’S HEALTH CARE, 30(1), 27–41Copyright © 2001, Lawrence Erlbaum Associates, Inc.

Requests for reprints should be sent to Simon Rietveld, Department of Psychology, Roetersstraat 15,1018 WB Amsterdam, The Netherlands. E-mail: [email protected]

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struction is necessary for proper use of bronchodilator medication, as well as foravoiding asthma-provoking situations in time (Strunk, 1987). Moreover, symptomperception might be a key issue in perceived control over symptoms and a determi-nant of proper coping with asthma (Creer, 1987).

Adult studies have shown an often striking discordance between lung functionand dyspnea. There exists usually no linear relation between lung function anddyspnea (Wolkove et al., 1992). In the study by Rubinfeld and Pain (1976), 15% ofadults with asthma were not able to perceive induced airway obstruction of 50%reduction in lung function. Patients with asthma might report themselves symptomfree in the midst of an asthma attack or conversely complain of dyspnea withoutairway obstruction (Barnes, 1992; Burdon, Juniper, Killian, Hargreave, & Camp-bell, 1982; Cote, LeBlanc, & Boulet, 1987; Fritz, Klein, & Overholser, 1990; Shim& Williams, 1980; Turcotte, Corbeil, & Boulet, 1990).

The discordance between the objective and subjective symptoms of asthma usu-ally has been attributed to receptor impairment associated with airwaypathophysiology (McFadden, Kiser, & de Groot, 1973). Chronic inflammatory pro-cesses, associated with pulmonary edema and excessive mucus secretion, are foundin the airways of adults with asthma, notably often without clinical manifestations(Clark, Godfrey, & Lee, 1992). These processes could interfere with receptor sensi-tivity and the afferent signals underlying symptom perception (Tack, Altose, &Cherniack, 1982). Several studies have suggested that subtle differences in airwaypathophysiology, caused by different asthma-provoking stimuli, also are involvedin poor symptom perception (Marks et al., 1996; Roisman, Peiffer, Lacronique, LeCae, & Dusser, 1995). Other research has suggested that neuropsychological devia-tions might explain blunted perception of airway obstruction in particular patients(Barnes,1994;Kikuchietal., 1994).The influenceonsymptomperceptionofdiffer-ent substances causing or relieving airway obstruction is still disputed (Higgs &Laszlo, 1996; Marks et al., 1996).

However, irrespective of underlying sensory information, dyspnea seems to bea symptom often lacking in specificity (Skevington, Pilaar, Routh, & MacLeod,1997). Contemporary models on the etiology of dyspnea propose that a dyspnearesponse is instigated by (a) increased effort of respiratory muscles, (b) excess ofarterial carbon dioxide, or (c) hypoxemia (Banzett et al., 1990; Campbell, Freed-man, Clark, Robson, & Norman, 1967). These models cannot explain extremesymptom-perceptual inaccuracy, as described earlier (Adams, Lane, Shea,Cockcroft, & Guz, 1985; Teramoto, 1995).

Recent psychological studies have shown that cognition, situation, and nega-tive emotions substantially influence symptom-perceptual accuracy as reflected indyspnea magnitude (Rietveld, 1998; Rietveld & Brosschot, 1999). Children withasthma in a physical exercise setting used false lung function information and falserespiratory sounds in their evaluation of asthma severity and reported highdyspnea, irrespective of actual airway obstruction (Rietveld, Kolk, Colland, &Prins, 1997; Rietveld, Kolk, & Prins, 1996). A lack of concentration also has been

28 RIETVELD, PRINS, COLLAND

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claimed to be influential in poor symptom perception (Noseda, Schmerber,Prigogine, & Yernault, 1992). However, distraction also might improve the per-ceptual accuracy by diminishing the number of false positive responses (Rietveld,Kolk, Prins, & Van Beest, 1997). Jones (1992) emphasized the impact of psycho-logical elaboration of illness experiences on subsequent symptom perception. Asingle experience with airflow obstruction influences dyspnea during followingattacks of airway obstruction (Wilson & Jones, 1990). Differences in dyspnea alsoare related to perceived control over symptoms—for example, trust in the effec-tiveness of medication (Rietveld, 1997; Wigal et al., 1993).

Negative emotions might play a key role in both symptom perception anddyspnea. First, emotional arousal interferes with accurate symptom perception(Hudgel, Cooperson, & Kinsman, 1982). Second, negative emotions overlap withdyspnea and might directly enhance its magnitude (Spinhoven, Van Peski-Oosterbaan, VanderDoes, Willems, & Sterk, 1997; Wilson & Jones, 1991). Third,negative emotions can be interpreted in terms of asthma symptoms (Dirks & Schraa,1983). Fourth, emotions associated with asthma may trigger asthma-congruent in-terpretation of vague or ambiguous sensory information in terms of anticipateddyspnea (Rietveld & Prins, 1998).

The proposition of psychological influences in symptom perception does notrule out the likelihood of pathophysiology affecting overall perceptual accuracybut often might explain inaccurate symptom perception. This addresses both ex-tremes of symptom perception: blunted perception and overperception of airwayobstruction, manifested in either absence of dyspnea during airway obstruction orexcessive dyspnea without airway obstruction (Rietveld & Brosschot, 1999). Atfirst glance, psychological influences seem to be more apparent in overperceptionthan in blunted perception. However, impaired perceptual capacity cannot explainwhy young children with lesser degrees of asthma are as vulnerable to blunting asare adults with severe asthma (Spina, 1996; Tack et al., 1982).

The aim of this study was to investigate the accuracy of symptom perception asa function of asthma severity in children and adolescents. Specifically, this studyaddressed the link between dyspnea magnitude and lung function, asthma severity,and airway hyperresponsiveness during histamine-induced and exercise-inducedairway obstruction. Furthermore, the predictive value of relevant variables withrespect to dyspnea magnitude was investigated.

EXPERIMENT 1

Method

Participants

A total of 30 children and adolescents with asthma (19 boys and 11 girls, ages 8–18years [M = 12.1, SD = 3.1]) took part in a histamine provocation test. It was not pos-

SYMPTOM PERCEPTION AND ASTHMA SEVERITY 29

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sible, either practically or ethically, to submit children without asthma to histamineinhalation. The participants were residents of the Heideheuvel Asthma Center atHilversum, The Netherlands. The study was approved by the ethical medical boardof the Asthma Center, and parents signed informed consent. The intake criteria in-cluded the following: (a) a recent doctor’s diagnosis of asthma, (b) prescribed med-ication fitting a classification of asthma severity according to the criteria of the Brit-ish Thoracic Society (1993), and (c) confirmed airway hyperresponsiveness viaairway provocation testing.

The severity of asthma was evaluated according to the scoring system of theBritish Thoracic Society (1993). There were 17 children and adolescents with a di-agnosis of severe asthma, treated with oral corticosteroids or large doses (800mcg) of inhaled corticosteroids and long-acting and short-acting bronchodilators.Six children were diagnosed with moderate–severe asthma, and they were treatedwith 400–800 mcg inhaled corticosteroids and long-acting and short-acting bron-chodilators. There were 2 children with moderate asthma, and they used smalldoses of inhaled corticosteroids and bronchodilators. Two children were diag-nosed with moderate–mild asthma and were treated with ipratropiumbromide, so-dium cromogliquate, and bronchodilators. Three children had mild asthma, andthey used bronchodilators when needed. According to the test protocol, the partici-pants were not allowed to take medication on the morning of testing. This waschecked by the assistants of the asthma center.

Procedure: Histamine Provocation Test

The aim of the provocation test was to induce airway obstruction, as defined by a re-duction in lung function (forced expiratory volume in 1 sec [FEV1]) of > 20%. Thisroutine clinical test was performed according to a structured protocol to assess thedegree of airway hyperresponsiveness. Histamine phosphate was prepared in arange of eight doubling concentrations from .25 to 32 mg/ml. Saline and the solu-tions of histamine were administered through a De Vilbiss (Jaeger, Germany) 646nebulizer with a gauged output of .13 mg/ml. The nebulizer was mounted within avalve box within an aerosol filter. The nebulization time was 30 sec, during whichthe participants were instructed to breathe quietly through the mouthpiece whileseated and wearing a nose clip. The test started with inhalation of a saline bufferaerosol, followed by the histamine concentrations. The lung function was mea-sured within 30 sec of each inhaled dose. When the lung function was reduced, itsassessment was repeated after 90 and 180 sec. The test was terminated when thelung function indicated a reduction of > 20% or after administration of the finalavailable histamine dose. A bronchodilator drug (two puffs of a β agonist) was ad-ministered for relief of airway obstruction to patients with a reduction in lung func-tion of > 20%.


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Measures

Assessment of airway obstruction. Airway obstruction was measured bylung-function testing with a pneumotachograph (Pneumoscreen II, Erich Jaeger,Wurzburg, Germany) and expressed as FEV1. There were three trials, and the high-est value was used for analysis. The lung function values recorded during pretestand after the final histamine dose were used for analysis. This comprised the abso-lute FEV1 and the percentage of FEV1 predicted for a child of similar sex, age,weight, and height.

Assessment of dyspnea. Dyspnea was measured at pretest and after hista-mine inhalation. Dyspnea was defined and explained to the participants as laboredbreathing, shortness of breath, tightness of the chest, or wheeziness. The termdyspnea in the Dutch language (benauwdheid) is clear in itself and a characteristicof the major subjective sensation during an asthma exacerbation. The degree ofdyspnea was marked by the participants on a self-report Likert-type scale. This wasa horizontal line with 10 scale points, ranging from 0 (no dyspnea) to 9 (most severedyspnea). The participants had previous experience with the scale. Former studies,conducted in an exercise setting, showed that a reduction in lung function of > 20%coincided with a mean rise in dyspnea of 2.5 scale points (cf. Quirk & Jones, 1990;Rietveld et al., 1996; Sly, Landau, & Weymouth, 1985).

Results

There were 26 children and adolescents with a reduction in lung function of > 20%after histamine inhalation, and 4 patients with a reduction of ≤ 20%; the latter datawere not statistically analyzed because the number of patients was too small. Thehistamine concentration causing the reduction of > 20% varied from 1 to 32 mg/ml(M = 8, SD = 10). The mean lung function in participants with a reduction in lungfunction of > 20% after histamine inhalation was reduced with 29%, which coin-cided with a mean rise in dyspnea of 4.2 scale points (the means and standard devia-tions are presented in Table 1).

Pearson product moment correlation coefficients were computed between rele-vant variables and showed that lung function, dyspnea and parameters of asthmaseverity (prescribed medication, airway hyperresponsiveness), and age were notsignificant (Table 2).

A multiple regression analysis was conducted to test the influence of relevantvariables on dyspnea. This test showed that only 16% of the variance in dyspneaafter histamine inhalation could be explained by a set of eight predictors1 (multiple


1Pretest dyspnea, pretest and posthistamine lung function, histamine threshold, severity of asthma,age, sex, and ethnic background.

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R = .40, p = .01). None of the individual predictors met the significance criterion ofp < .05. Consequently, variance in dyspnea could not be explained with these ob-jective variables.

EXPERIMENT 2

Method

Participants

A total of 64 children and adolescents with asthma and 30 without asthma (62 boysand 32 girls ages 7–17 years [M = 11.6, SD = 2.9]) performed a physical exercise


TABLE 1Means and Standard Deviations of Dyspnea, Lung Function, and Percentage Lung

Function Predicted During Histamine Challenge Test

Pretesta Posthistaminea Posttesta

Dependent Measures M SD M SD M SD

D 0.9 1.2 5.1 2.0 1.7 1.9FEV1 2.16 0.70 1.46 0.58 2.03 0.71% 91 13 62 15 86 17

Note. Pretest = baseline assessment before histamine exposure; Posthistamine = assessmentimmediately after the final histamine dose; Posttest = assessment 10 min after bronchodilatormedication; D = dyspnea; FEV1 = forced expiratory volume in 1 sec.

TABLE 2Pearson Correlations Between Dyspnea With Lung Function and Percentage

Lung Function Predicted of Children and Adolescents With AsthmaDuring Histamine Challenge Test

Dependent Measures Pretesta Posthistaminea Posttesta Totala

r1 0.11 0.09 –0.04 0.11r2 –0.04 –0.01 –0.18 –0.05

Note. Pretest = baseline assessment before histamine exposure; Posthistamine = assessmentimmediately after the final histamine dose; Posttest = assessment 10 min after bronchodilatormedication; Total = correlation over different assessments; r1 = correlation between dyspnea and lungfunction; r2 = correlation between dyspnea and percentage lung function predicted.

an = 26.

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task. The children and adolescents with asthma were residents of the HeideheuvelAsthma Center, Hilversum, The Netherlands, or enrolled via general physicians.All parents signed informed consent. With respect to intake criteria, compare toParticipants section in Experiment 1.

With 4 patients excluded from analysis because of a poor pretest lung function,there were 14 children and adolescents with a diagnosis of severe asthma, treatedwith oral corticosteroids or large doses (800 mcg) of inhaled corticosteroids andlong-acting and short-acting bronchodilators. Eight participants were diagnosedwith moderate–severe asthma and were treated with inhaled 400–800 mcgcorticosteroids and long-acting and short-acting bronchodilators. Fourteen partici-pants with moderate asthma used small doses of inhaled corticosteroids and bron-chodilators. Ten children and adolescents were diagnosed with moderate–mildasthma and were treated with ipratropiumbromide, sodium cromogliquate, andbronchodilators. Another 14 participants had mild asthma and used only broncho-dilators when needed. Parents and participants were informed that bronchodilatorswere not to be used on the day of the test. The participants without asthma had nohistory of respiratory disease.

Procedure: Physical Exercise Task

The aim of the exercise task was to induce a mild degree of airway obstruction, asdefined by a reduction in lung function. Hence, the lung function was measured be-fore and after the test. In patients with airway obstruction who received medication,there was a third lung-function assessment. The task was performed indoors in anair-conditioned environment with optimal temperature and humidity. The tempera-ture at 5 ft (1.52 m) above ground level ranged from 68 to 70 °F, and humidity wasbetween 60% and 64%. The task consisted of free running, and the participantscould choose speed of running. They ran through a broad corridor in the buildinguntil a heartbeat rhythm of 180 bpm was indicated by the sound signal of a controldevice that was strapped around the chest of each child (Polar Edge, SemexMedische Techniek, Nieuwegein, The Netherlands). The participants remainedseated for 5 min after exercise. A bronchodilator drug (two puffs of a β agonist) wasadministered for relief of airway obstruction to children and adolescents with a re-duction in lung function of > 20% (Anderson, 1985; Eggleston & Guerrant, 1976;Haynes, Ingram, & McFadden, 1976).

Measures

Assessment of airway obstruction and dyspnea. Airway obstructionand dyspnea were measured pretest and postexercise by using the same techniqueas in Experiment 1. A third assessment (posttest) followed only after administrationof medication to patients with airway obstruction.


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Results

The pretest lung function of 4 patients did not permit testing (FEV1 of < 57% of pre-dicted), leaving 60 children and adolescents with asthma for the physical exercisetask. There were 8 patients with a reduction of > 20% in lung function after physicalexercise, 15 with a reduction of ≤ 20% but > 10%, and 37 with a reduction of ≤ 10%.Children and adolescents without asthma had a reduction in lung function of <10%. The mean lung function in children and adolescents with a reduction in lungfunction of > 20% after physical exercise was reduced with 30%, which coincidedwith a mean rise in dyspnea of 2.5 scale points.

Table 3 shows the means and standard deviations of dyspnea. Particularly inter-esting is the difference between participants with asthma, but without airway ob-struction, and participants without asthma. Pearson correlations among lungfunction, dyspnea, and other relevant variables did not reach the significance levelof p < .05 (Table 4).


TABLE 3Means and Standard Deviations of Dyspnea, Lung Function, and Percentage Lung

Function Predicted of Children and Adolescents With Asthma (Groups A–C) and WithoutAsthma (Group D) During Physical Exercise Task

Pretest Postexercise Posttest

Dependent Measures M SD M SD M SD

Group Aa

D 1.0 1.2 3.5 3.7 2.0 2.4FEV1 2.28 0.46 1.43 0.49 1.93 0.75% 81 17 51 16 69 21

Group Bb

D 1.3 1.0 3.6 1.9 — —FEV1 2.25 0.82 1.80 0.71 — —% 81 16 65 15 — —

Group Cc

D 1.4 1.1 2.5 2.1 — —FEV1 2.12 0.66 2.09 0.63 — —% 94 14 93 16 — —

Group Dd

D 0.4 0.8 0.7 1.0 — —FEV1 2.81 0.82 2.79 0.86 — —% 97 12 96 14 — —

Note. Dashes indicate Posttest did not take place because participants needed no medication.Pretest= baseline assessment before exercise; Postexercise = assessment after running; Posttest = assessment10 min after bronchodilator medication (only in children who received medication after significantairway obstruction [Group A]); D = dyspnea; FEV1 = forced expiratory volume in 1 sec.

an = 8. bn = 15. cn = 37. dn = 30.

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An analysis of covariance was conducted to test differences between partici-pants with and without asthma. To correct for differences in lung function, theFEV1 entered this analysis as covariate. There were significant Test and Conditioneffects, F(1, 58) = 12.34, p < .001, and F(1, 58) = 101.13, p < .001, respectively.The interaction effect of Test × Condition was also significant, F(2, 58) = 16.25, p< .001. These results indicated that dyspnea increased significantly from pretest topostexercise, particularly in participants with asthma. Overall, participants withasthma reported more dyspnea than did participants without asthma, particularlyafter exercise. The covariate lung function (FEV1) was not significantly influen-tial in these tests (p = .039).

A multiple regression analysis showed that 53% of the variance in dyspnea af-ter physical exercise could be explained by a set of seven predictors2 (multiple R =.73, p = .01). Only three variables were of individual significant influence: pretestdyspnea (β = 0.55, p = .01), postexercise lung function (β = –0.76, p = .01), and sex(β = –0.32, p = .02). The pretest lung function came close to significance (β = .59, p= .09). This suggested that boys with relatively high pretest dyspnea and a high re-duction in lung function were likely to report high dyspnea after physical exercise.The other predictors were not of substantial influence: age, severity of asthma, andethnic background.


TABLE 4Pearson Correlations Between Dyspnea With Lung Function and Percentage Lung

Function Predicted of Children and Adolescents With Asthma (Groups A–C), and WithoutAsthma (Group D) During Physical Exercise Task

Reduction ofLung Function Group Correlation Pretest Postexercise Posttest Total

> 20% A r1 –0.14 –0.49 –0.36 –0.26n = 8 r2 –0.02 –0.45 –0.36 –0.16≤ 20% B r1 –0.16 –0.21 0.05 –0.18n = 15 r2 0.22 0.36 –0.10 –0.22≤10% C r1 0.04 –0.07 — 0.02n = 37 r2 –0.02 –0.07 — –0.10

D r1 –0.16 –0.21 — –0.19n = 30 r2 0.22 0.36 — 0.20

Note. Dashes indicate Posttest did not take place because participants needed no medication.r1 =correlation between dyspnea and lung function; r2 = correlation between dyspnea and percentage lungfunction predicted; Pretest = baseline assessment before exercise; Postexercise = assessment afterrunning; Posttest = assessment 10 min after bronchodilator medication; Total = correlation overdifferent assessments.

2See Footnote 1 with the exception of histamine threshold.

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DISCUSSION

The data of the two experiments showed that dyspnea did not significantly relate toparameters of asthma severity in children and adolescents during either histamine-or exercise-induced airway obstruction. The magnitude of dyspnea did not corre-late with lung function, prescribed medication, or airway hyperresponsiveness tohistamine. The data suggested that participants with asthma but without reductionin lung function reported more dyspnea than normal controls. The differences indyspnea between participants were poorly explained by predictor variables such asage, sex, and ethnic background.

The results indicated that magnitude of dyspnea (and hence the accuracy ofsymptom perception) was independent of objective parameters of asthma severity.Although correlations between dyspnea and lung function were not significantthroughout the study, the data suggested that the highest discordance existed duringposttest assessment, which confirmed previous clinical observations (McFadden etal., 1973; Rubinfeld & Pain, 1976). Secondary symptoms and psychological factorscould be accounting for huge scatter in posttest dyspnea responses. Several re-searchers emphasized that the discordance between lung function and dyspnea hasnotbeenexplainedsatisfactorily (Jones,1992;Pratter&Barter,1991).McFaddenetal. (1973) attributed the discordance between lung function and dyspnea to persis-tent obstruction in peripheral airways compromising lung function but insufficientfor a dyspnea response. Teramoto (1995), among other researchers, focused onchemical substances influencing dyspnea magnitude. Rietveld (1998) emphasizedthat patients have learned to attend to relevant information that might influence theirsymptom perception, regardless of objective, physical factors.

There are at least three limitations to these conclusions. First, there is uncer-tainty about the classification of asthma severity. In the current consensus of pul-monary physicians, this classification is based on prescribed medication.Although prescription follows the severity and persistence of symptoms, differentphysicians may interpret signs and symptoms differently. This problem was notimportant in Experiment 1 (a team of physicians followed strict rules) but mighthave been in Experiment 2 (different physicians). Additional information aboutthe asthma severity of these samples is available from baseline lung function dataand the sensitivity of the airways for histamine and exercise, respectively. In thisrespect, the data suggested that none of these factors related to dyspnea magnitude.A second problem was that bronchodilator medication could not be checked in Ex-periment 2. Participants who (against instructions) used medication before the ex-periment could have been less vulnerable to airway obstruction. This could explainwhy only a few participants developed severe airway obstruction. As a third con-cern, several secondary symptoms were different in the two experiments. Excessof saliva and mucus were a characteristic of histamine inhalation, triggering coughand frequent swallowing. Sighing, heart pounding, and fatigue were typical symp-


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toms after physical exercise. These secondary symptoms could account for vari-ance in dyspnea during histamine provocation and physical exercise, respectively.In other words, variance in dyspnea could be related to secondary symptoms ratherthan psychological factors influencing dyspnea magnitude.

These results confirmed the findings of a study by Janson-Bjerklie, Ruma,Stulbarg, Kohlman, and Carrieri (1987) that pretest dyspnea was predictive ofdyspnea during airway obstruction, but our data refuted their conclusion thatwomen score higher than men. The difference might refer to the distinction be-tween children and adults. Our study did not show a significant effect of age,whereas Janson-Bjerklie et al. (1987) found a significant negative correlation be-tween age and dyspnea, with young participants scoring higher than older ones.The difference between the studies would suggest that psychological and situa-tional factors are more important than age itself. Burdon and colleagues (1982) ob-served that adults with a lowered baseline lung function were less accurate insymptom perception during the height of induced asthma than patients with a base-line lung function within the normal range. The results of our study did not supportthis. Burdon et al. (1982) observed that patients with a high tolerance for histaminereported more dyspnea than patients with a low tolerance, which was not con-firmed by out data. Patients with highly sensitive airways generally would be ex-posed to asthma attacks more often, which could influence their symptomperception (Yellowlees & Ruffin, 1989). On the other hand, children and adoles-cents with a high tolerance for histamine received more concentrations of hista-mine than did those with low tolerance. This implies that the former were exposedlonger to the experimental regime, which could have been reflected in higher dis-tress, influencing the accuracy of symptom perception and enhancing dyspnea(Rietveld & Prins, 1998; Wilson & Jones, 1991).

These results suggested that children with relatively mild asthma were as inac-curate in symptom perception as were adults with very severe asthma in previousstudies. In other words, inaccurate symptom perception in asthma is probably notrelated to impaired perception due to severe pulmonary pathology (Wolkove et al.,1992). It was surprising that some participants did not report an increase indyspnea during marked reductions in lung function whereas others reported highdyspnea during a lung function within their usual range. It is intriguing that a17-year-old girl with mild asthma scored zero with a reduction in lung function of29%, and a 10-year-old boy with mild–moderate asthma scored zero with a reduc-tion of 18%. Because many children and adolescents seemed to be distressed, thereason for mild scoring on dyspnea remained unclear. Consequently, it is unlikelythat the discordance between dyspnea and objective symptoms of asthma shouldbe attributed to airway pathophysiology. Because asthma is potentially alife-threatening condition, all available asthma-related information is extensivelyelaborated, facilitating the impact of cognitive, emotional, and situational factors(Rietveld & Brosschot, 1999). Absence of dyspnea during airway obstruction in


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adolescents who are aware of airway obstruction has been attributed to absence ofanxiety or a high sense of perceived control over symptoms (Rietveld, 1997). Thisproposition could be an alternative explanation for the so-called impaired symp-tom perception in asthma. Although lack of concentration could explain bluntedsymptom perception in everyday situations, this could hardly be the case duringinduced airway obstruction in a laboratory with participants eagerly followingeach experimental sequence and actively introspecting (Noseda et al., 1992).

The major psychological determinant of excessive magnitude of dyspnea mightbe selective perception of symptoms, enhancing the magnitude of self-reportedsymptoms, as well as the likelihood of biased symptom perception (Pennebaker,1982; Pennebaker & Skelton, 1981). Two mechanisms could facilitate the impactof psychological and situational factors: (a) false interpretation of general physicalsymptoms as symptoms of airway obstruction and (b) secondary symptoms andtest-related emotions enhancing overall distress (Carrieri, Kieckhefer,Janson-Bjerklie, & Souza,1991; Dirks & Schraa, 1983; Rietveld, Everaerd, & VanBeest, 1999; Rietveld & Prins, 1998).

Dyspnea seems to be a subjective experience with its magnitude psychologi-cally determined. This study subscribes to the importance of multidisciplinary re-search procedures. To understand dyspnea in relation to airway obstruction,studies should be conducted with a wide spectrum of subjective and objective vari-ables assessed in parallel.

IMPLICATIONS FOR PRACTICE

Children’s reports of dyspnea are less reliable than currently believed. Adequateself-management of asthma in many children and adolescents is probably only pos-sible by means of frequent use of the more objective peakflow meter at the first signof dyspnea—first as a guideline for general behavior and second as a basis forchanging medication. However, the peakflow also is influenced by subjective fac-tors; for example, children use them intermittently, and children are often carelessin the proper handling. In patients with a questionable reliability in the usage of pre-scribed medication, as well as in youngsters with confirmed poor symptom percep-tion, we advocate daily use of corticosteroids or other anti-inflammatory medica-tion instead of if-needed bronchodilators. Health care professionals should beaware of situations in which patients with asthma are vulnerable to biased symptomperception—for instance, when they are in a situation in which symptoms previ-ously occurred or when they are stressed or emotional. Conclusions about theirasthmatic condition under such circumstances should be based on more objectivepeakflow assessment rather than merely subjective evaluation, particularly withyoung children. Inaccurate symptom perception implies that children often are un-aware of their asthmatic state. Health care professionals should be suspicious re-garding children with unexplained fatigue or irritability. Wheezing respiratory


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sounds are often audible near the patient, and persistent cough also might indicatean exacerbation of asthma. Fluctuations in symptoms often might delay a proper di-agnosis and treatment. We stress the importance of multidisciplinary asthma man-agement, which should include a variety of medical and psychological factors.

ACKNOWLEDGMENTS

This study was financially supported by the Netherlands Asthma Foundation.We thank Alice Scholte and Irma Toonen for a fine job during lung-function

testing. We also thank Irma Toonen for general assistance throughout the study.Special thanks to Cedric Sands for commenting on drafts of the article and JamesBoutos for final proofreading.

REFERENCES

Adams, L., Lane, R., Shea, S. A., Cockcroft, A., & Guz, A. (1985). Breathlessness during differentforms of ventilatory stimulation: A study of mechanisms in normal subjects and respiratory patients.Clinical Science, 69, 663–672.

Anderson, S. D. (1985). Issues in exercise-induced asthma. Journal of Allergy and Clinical Immunol-ogy, 76, 763–772.

Banzett, R. B., Lansing, R. W., Brown, R., Topulos, G. P., Yager, D., Stelle, S. M., Londoo, B., Loring,S. H., Reid, M. B., Adams, L., & Nations, C. S. (1990). “Air hunger” from increased PCO2 persistsafter complete neuromuscular block in humans. Respiration Physiology, 81, 1–18.

Barnes, P. J. (1992). Poorly perceived asthma [Editorial]. Thorax, 47, 408.Barnes, P. J. (1994). Blunted perception and death from asthma [Editorial comments]. New England

Journal of Medicine, 330, 1383–1384.British Thoracic Society. (1993). Guidelines on the management of asthma. Thorax, 48, 1–24.Burdon, J. G. W., Juniper, E. F., Killian, K. J., Hargreave, F. E., & Campbell, E. J. M. (1982). The per-

ception of breathlessness in asthma. American Review of Respiratory Disease, 126, 825–828.Campbell, E. J. M., Freedman, S., Clark, T. J. H., Robson, J. G., & Norman, J. (1967). The effect of mus-

cular paralysis induced by tubocurarine on the duration and sensation of breath-holding. ClinicalScience, 32, 425–432.

Carrieri, V. K., Kieckhefer, G., Janson-Bjerklie, S., & Souza, J. (1991). The sensation of pulmonarybreathlessness in school-age children. Nursing Research, 40, 81–85.

Clark, T. J. H., Godfrey, S., & Lee, T. H. (1992). Asthma. London: Chapman & Hall.Cote, J., LeBlanc, P., & Boulet, L. P. (1987). Perception of bronchospasm in normal and asthmatic sub-

jects. American Review of Respiratory Disease, 135, 231.Creer, T. L. (1987). Self-management in the treatment of childhood asthma. Journal of Allergy and Clin-

ical Immunology, 80, 500–506.Dirks, J. F., & Schraa, J. C. (1983). Patient mislabelling of symptoms and rehospitalization in asthma.

Journal of Asthma, 20, 43–44.Eggleston, P. A., & Guerrant, J. L. (1976). A standardized method of evaluating exercise-induced

asthma. Journal of Allergy and Clinical Immunology, 58, 414–425.Fritz, G. K., Klein, R. B., & Overholser, J. C. (1990). Accuracy of symptom perception in childhood

asthma. Developmental Behavior in Pediatrics, 11, 69–72.


Dow

nloa

ded

by [

Sim

on F

rase

r U

nive

rsity

] at

19:

08 1

8 N

ovem

ber

2014

Haynes, R. L., Ingram, R. H., & McFadden, E. R. (1976). An assessment of the pulmonary response toexercise in asthma and an analysis of the factors influencing it. American Review of Respiratory Dis-ease, 114, 739–752.

Higgs, C. M. B., & Laszlo, G. (1996). Influence of treatment with beclomethasone, cromoglycate, andtheophylline. Clinical Science, 90, 227–234.

Hudgel, H. D., Cooperson, D. M., & Kinsman, R. A. (1982). Recognition of added resistive loads inasthma; the importance of behavioral styles. American Review of Respiratory Disease, 126,121–125.

Janson-Bjerklie, S., Ruma, S. S., Stulbarg, M., Kohlman, K., & Carrieri, V. K. (1987). Predictors ofbreathlessness intensity in asthma. Nursing Research, 36, 179–183.

Jones, P. W. (1992). Breathlessness perception in airways obstruction. European Respiratory Journal,5, 1035–1036.

Kikuchi, Y., Okabe, S., Tamura, G., Hida, W., Homma, M., Shirato, K., & Takashima, T. (1994).Chemosensitivity and perception of dyspnea in patients with a history of near-fatal asthma. NewEngland Journal of Medicine, 330, 1329–1334.

Marks, G. B., Yates, D. H., Sist, M., Ceyhan, B., De Campos, M., Scott, D. M., & Barnes, P. J. (1996).Respiratory sensation during bronchial provocation testing with methacholine, sodium metabisul-phite, and adenosine monophosphate. Thorax, 51, 793–798.

McFadden, E. R., Kiser, R., & de Groot, W. J. (1973). Acute bronchial asthma; relations between clini-cal and physiological manifestations. New England Journal of Medicine, 288, 221–225.

Noseda, A., Schmerber, J., Prigogine, T., & Yernault, J. C. (1992). Perceived effect on shortness ofbreath of an acute inhalation of saline or terbutaline: Variability and sensitivity of visual analoguescale in patients with asthma and COPD. European Respiratory Journal, 5, 1043–1053.

Pennebaker, J. W. (1982). The psychology of physical symptoms. New York: Springer.Pennebaker, J. W., & Skelton, J. A. (1981). Selective monitoring of physical sensations. Journal of Per-

sonality and Social Psychology, 41, 213–223.Pratter, M. R., & Barter, T. (1991). Dyspnea: Time to find the facts. Chest, 100, 1187.Quirk, F. H., & Jones, P. W. (1990). Patients’ perception of distress due to symptoms and effects of asthma

on daily living and an investigation of possible influential factors. Clinical Science, 79, 17–21.Rietveld, S. (1997). Habituation to prolonged airflow obstruction. Journal of Asthma, 34, 133–140.Rietveld, S. (1998). Symptom perception in asthma, a multidisciplinary review. Journal of Asthma, 35,

137–146.Rietveld, S., & Brosschot, J. F. (1999). Current perspectives on symptom perception in asthma; a biolog-

ical and psychological review. International Journal of Behavioral Medicine, 6, 120–135.Rietveld, S., Everaerd, W., & Van Beest, I. (1999). Can biased symptom perception explain false-alarm

choking sensations? Psychological Medicine, 29, 121–126.Rietveld, S., Kolk, A. M. M., Colland, V. T., & Prins, P. J. M. (1997). The influence of respiratory

sounds on breathlessness in children with asthma: A symptom-perception approach. Health Psy-chology, 16, 547–553.

Rietveld, S., Kolk, A. M. M., & Prins, P. J. M. (1996). The influence of lung function information onself-reports of dyspnea by children with asthma. Journal of Pediatric Psychology, 21, 367–377.

Rietveld, S., Kolk, A. M. M., Prins, P. J. M., & Van Beest, I. (1997). The influence of external stimula-tion on airflow detection by children with and without asthma. Psychology and Health, 12, 553–563.

Rietveld, S., & Prins, P. J. M. (1998). The relationship between negative emotions and acute objectiveand subjective symptoms of childhood asthma. Psychological Medicine, 28, 407–415.

Roisman, G. L., Peiffer, C., Lacronique, J. G., Le Cae, A., & Dusser, D. J. (1995). Perception of bronchialobstruction in asthmatic patients. Relationship with bronchial eosinophilic inflammation and epithe-lial damage and effect of corticosteroid treatment. Journal of Clinical Investigation, 96, 12–21.

Rubinfeld, A. R., & Pain, M. C. F. (1976). Perception of asthma. The Lancet, 2, 882–884.


Dow

nloa

ded

by [

Sim

on F

rase

r U

nive

rsity

] at

19:

08 1

8 N

ovem

ber

2014

Shim, C. S., & Williams, M. H. (1980). Evaluation of the severity of asthma: Patients versus physicians.American Journal of Medicine, 68, 111–113.

Skevington, S. M., Pilaar, M., Routh, D., & MacLeod, R. D. (1997). On the language of breathlessness.Psychology and Health, 12, 677–689.

Sly, P. D., Landau L. L., & Weymouth, R. (1985). Home recording of peak expiratory flow rates and per-ception of asthma. American Journal of Diseases in Childhood, 18, 479–482.

Spina, D. (1996). Airway sensory nerves: A burning issue in asthma? Thorax, 51, 335–337.Spinhoven, P., Van Peski-Oosterbaan, A. S., VanderDoes, A. J. W., Willems, L. N. A., & Sterk, P. J.

(1997). Association of anxiety with perception of histamine induced bronchoconstriction in patientswith asthma. Thorax, 52,149–152.

Strunk, R. C. (1987). Asthma death in childhood, identification of patients at risk and intervention. Jour-nal of Allergy and Clinical Immunology, 80, 472–505.

Tack, M., Altose, M. D., & Cherniack, N. S. (1982). Effect of aging on the perception of resistiveventilatory loads. American Review of Respiratory Disease, 126, 463–467.

Teramoto, S. (1995). Perception of breathlessness: Clinical perspective [Letter to the editor]. EuropeanRespiratory Journal, 8, 338.

Turcotte, H., Corbeil, F., & Boulet, L. (1990). Perceptions of breathlessness during bronchoconstrictioninduced by antigen, exercise and histamine challenges. Thorax, 45, 914–918.

Wigal, J. K., Stout, C., Brandon, M., Winder, J. A., McConnaughy, K., Creer, T. L., & Kotses, H. (1993).The Knowledge, Attitude, and Self-Efficacy Asthma Questionnaire. Chest, 104, 1144–1148.

Wilson, R. C., & Jones, P. W. (1990). Influence of prior ventilatory experience on the estimation ofbreathlessness during exercise. Clinical Science, 78, 149–153.

Wilson, R. C., & Jones, P. W. (1991). Differentiation between the intensity of breathlessness and the dis-tress it evokes in normal subjects during exercise. Clinical Science, 80, 65–70.

Wolkove, N., Dajozman, E., Coalacone, A., Kriesman, H., Peiffer, C., Toumi, M., Razzouk, H., Marsac,J., & Lockhart, J. (1992). Relationship between spontaneous dyspnoea and liability of airway ob-struction in asthma. Clinical Science, 82, 717–724.

Yellowlees, P. M., & Ruffin, R. E. (1989). Psychological defenses and coping styles in patients follow-ing a life-threatening attack of asthma. Chest, 95, 1298–1303.


Dow

nloa

ded

by [

Sim

on F

rase

r U

nive

rsity

] at

19:

08 1

8 N

ovem

ber

2014

accuracy of symptom perception in asthma and illness severity

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