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Anxiety sensitivity and panic attacks in an asthmatic population
Behov. Res. Thu. Vol. 32, No. 4, pp. 411418,
1994 Copyright cc 1994 Elsevier Science Ltd Printed in Great Britain. All rights reserved 0005-7967/94 $6.00 + 0.00
Pergamon
ANXIETY
SENSITIVITY AND PANIC ATTACKS ASTHMATIC POPULATION
RICHARD
E. CARR,
PAUL
M.
STUART Department
of psychiatry,
Robert
LEHRER,* M.
LAWRENCE
IN AN
L. RAUSCH
and
UMDNJ,
Piscataway,
HOCHRON
Wood Johnson Medical NJ 08854-5635, U.S.A.
School,
(Received 10 March 1993) Summary-The purpose of this study was to examine the relationship among anxiety sensitivity, the experience of frequent, spontaneous panic attacks, and pulmonary function in individuals with asthma. Ninety-three asthmatics participated by completing a battery of questionnaires and a spirometric assessment. Twenty-three percent of the asthmatics reported a history of spontaneous panic attacks with 9.7% reporting attacks that were severe and frequent enough to meet the DSM-IIIR criteria for panic disorder (PD). Anxiety sensitivity (ASI) scores, but not pulmonary function, was significantly related to PD. In addition, we compared the asthmatics (with and without PD) to 10 clinically diagnosed PD Ss without asthma and to 32 nonanxious, nonasthmatic controls on the ASI, the Body Sensations Questionnaire. and the Agoraphobic Cognitions Questionnaire. Whereas Ss with PD (asthmatic and nonasthmatic) displayed significant elevations on these measures compared to those without PD, the presence of asthma alone had no effect. The present study concurs with that of Porzelius et al. [BehaGur Research and Therapy, 30, 75-77 (1992)] in extending the validity of the cognitive model of PD to individuals with pulmonary disease.
INTRODUCTION
The study of asthma can be an important source for understanding the relative contributions of respiratory abnormalities and of cognitions to panic-related experiences (Carr, Lehrer & Hochron, 1992; Porzelius, Vest & Nochomovitz, 1992; Yellowlees, Alpers, Bowden, Bryant & Ruffin, 1987; Yellowlees, Haynes, Potts & Ruffin, 1988; Kinsman, Luparello, O’Banion & Spector, 1973). Asthma is a respiratory disease characterized by hyperreactive airways. The symptoms include wheezing and congestion, as well as hyperventilation (e.g. dyspnea, dizziness, racing heart), the last of which is common also to panic disorder (PD). Moreover, the catastrophic misinterpretation of physical sensations, particularly hyperventilation-induced sensations, is central to cognitive theories regarding the genesis and maintenance of PD (Clark, 1986; Beck, 1988). The experience of hyperventilation-induced dyspnea is also central to Ley’s dyspnea-fear theory of PD (Ley, 1989). In addition to sharing a number of physical symptoms, PD and asthma show a high incidence of comorbidity. For example, Kinsman et al. (1973) found that 42% of asthmatics reported that panic-fear occurred frequently with their asthma attacks. Yellowlees et al. (1987) found a high rate of anxiety disorders (34%) among a sample of 50 asthmatics in Australia, 12 (24%) of whom received a diagnosis of PD. In a follow-up study, approximately 12% of 49 asthmatic subjects (Ss) met the DSM-III (APA, 1980) criteria for PD as assessed by structured interview (Yellowlees et al., 1988). Whereas these studies document a higher than normal rate of panic among those with asthma, others have tried to explain it by searching for possible differences in pulmonary function or in cognitions between asthmatics with PD vs those without PD. For example, Porzelius et al. (1992) reported that 37% of a sample of 48 patients with chronic obstructive pulmonary disease (COPD) experienced panic attacks. Interestingly, although panickers did not differ from nonpanickers in either severity of their pulmonary disease or severity of shortness of breath, they were distinguished by more frequent agoraphobic cognitions and greater fear of body sensations. The data suggest *To whom
all reprint
requests
should
be addressed. 411
412
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E.
CARR
el al.
that COPD patients experience panic attacks because the symptoms are misinterpreted, not because of high generalized anxiety, depression, or more severe pulmonary impairment. By contrast, a previous study in this laboratory (Carr et al., 1992) found that panic-fear among asthmatics, but not among ADIS-R-diagnosed [Anxiety Disorders Interview Schedule-Revised (DiNardo & Barlow, 1988)] PD patients, was strongly related to severity ratings of dyspnea. These results suggest that dyspnea plays a more central role in the experience of panic-fear among asthmatics than it does among nonasthmatic PD patients. Despite interest in studying the interaction between respiratory symptoms and catastrophic cognitions among Ss with varying degrees of pulmonary disease, research in this area has lacked a critical measure of psychological vulnerability to panic-related phenomena: anxiety sensitivity. Anxiety sensitivity reflects an individual’s concerns about the consequences of experiencing anxiety-related symptoms. It is described by Reiss & McNally (1985) as a personality trait that increases an individual’s conditionability for fear [see Reiss (1991) for a review]. It is highly stable over time (Maller & Reiss, 1992) distinct from state and trait anxiety (Reiss, 1991) and better able to predict panic attack frequency and a history of PD than is generalized or trait anxiety (Reiss, Peterson, Gursky & McNally, 1986). In a study of 425 college students, Donnell & McNally (1990) found a significantly higher proportion of Ss reporting spontaneous panic attacks among those classified as high (32.4%) on the Anxiety Sensitivity Index (ASI) than among those classified as medium (15.6%) or low (5.1%). High AS1 Ss also reported more frequent treatment-seeking and a greater first-degree family history of panic than did others. In addition, high anxiety sensitivity has been shown to predict affective response to CO, inhalation better than Hamilton Anxiety scores, social anxiety, and depression (Rapee, Brown, Antony & Barlow, 1992); and, in one study of hyperventilation challenge, high anxiety sensitivity was a better predictor of response than was a history of panic attacks (Holloway & McNally, 1987; Donnell & McNally, 1989). Finally, since two-thirds of Ss with high anxiety sensitivity have never experienced a panic attack, prior experience of panic is not a necessary causal factor either of high anxiety sensitivity or of exaggerated reactions to biological challenges (Donnell & McNally, 1990). Reiss et al. (1986) conclude that in order to predict panic, it is more valuable to know what an individual expects to happen as a result of becoming anxious than it is to know how frequently they experience anxiety symptoms. This may explain the high rate of panic attacks and specifically PD among asthmatics. Asthmatics experience more symptoms of dyspnea and hyperventilation than do nonasthmatics, and sometimes these symptoms can be associated with life-threatening asthma exacerbations; however, not all asthmatics experience panic. Thus, panic attacks in this population may depend more on concerns about these sensations (i.e. anxiety sensitivity) than on the actual severity of the illness (i.e. objective measures of pulmonary function). Therefore, PD among persons with asthma should show a relationship to anxiety sensitivity that is similar to that previously found among nonasthmatics (e.g. Donnell & McNally, 1990); and asthmatics with PD should also show elevated scores on measures of catastrophic cognitions and fear of body sensations, relative to those without PD. The purpose of this study was twofold. First, to determine if a relationship exists between anxiety sensitivity and PD among persons with asthma. Second, to compare measures of panic-related cognitions among 4 groups: (1) asthma Ss without PD (AS); (2) asthma Ss who report the DSM-IIIR criteria for PD (AS-PD); (3) nonasthmatic, nonpanicking control Ss (Nor); and (4) PD patients who do not have asthma (PD). The study specifically addresses the following 4 questions: (1) Does the proportion of asthmatics who have PD increase as a function of anxiety sensitivity? (2) Do asthmatics with PD suffer from worse pulmonary function relative to asthmatics without PD? (3) Do asthmatics with PD report high ratings of panic-related cognitions than do those without PD? (4) Is asthma associated with high ratings of panic-related cognitions independent of the presence of PD?
Panic attacks and asthma
413
METHOD
A total of 13.5Ss participated in the study. The asthmatic sample consisted of 93 Ss (51 females) recruited via newspaper and radio advertisements, posted announcements, and physician referrals. They had an average age of 25.9 years (SD = 6.6). Diagnoses of asthma were made by a board-certified pulmonary physician on the basis of history, physical examination, spirometry, bronchodilator response to albuterol, and a diffusing capacity test. They were also screened to rule out medical diseases other than asthma. Thirty-two nonasthmatics (Nor group, 19 females) with an average age of 29.1 years (SD = ?.l), and who were screened to rule out a history of panic attacks or other psychiatric problems, were similarly recruited via posted announcements and newspaper advertisements. Finally, 10 nonasthmatic patients (PD group, 7 females) with a diagnosis of PD and an average age of 33.0 years (SD = 6.0) were recruited from physician referrals and newspaper advertisements. Diagnoses of PD according to DSM-IIIR criteria (APA, 1987) were confirmed by the ADIS-R (DiNardo & Barlow, 1988). Seven of the 10 PD patients were currently undergoing some form of mental health treatment. Three were receiving medication only, 3 were receiving a combination of medication and behavior therapy, and 1 was undergoing behavior therapy only. However, patients were included only if symptomatic during the previous month, as defined by significant daily worry about the occurrence of a panic attack, or report of at least 1 panic attack. Number of years since onset of PD ranged from 1 to 23 years. Excluding the patient with a 23-year history, the average number of years since first panic attack was 8.2. The group reported an average of 4.8 (SD = 3.8) panic attacks over the previous month with an average of 8.8 (SD = 2.0) symptoms per attack. Smokers were excluded from all groups, and nonasthmatic Ss were screened for abnormal pulmonary function. Dependent measwe~ Self-report. Patients completed a battery of questionnaires that included the Anxiety Sensitivity Index (ASI), the Agoraphobic Cognitions Questionnaire (ACQ), and the Body Sensations Questionnaire (BSQ). The AS1 is a valid and reliable l6-item questionnaire measuring an individual’s concerns about the consequences of experiencing anxiety symptoms (e.g. “It scares me when I become short of breath”, “When I notice my heart beating rapidly I worry that I may have a heart attack”). Items are rated on a 0- to 4-point Likert scale, with total scores ranging from 0 to 64 (Peterson & Reiss, 1987; Peterson & Heilbronner, 1987; Reiss et al., 1986; Foa, Steketee & Young, 1984). The ACQ and SSQ are companion scales developed by Chambless (Chambless, Caputo, Bright & Gallagher, 1984) for measuring the construct of fear of fear. The ACQ is a 1Citem scale assessing the presence of specific catastrophic thoughts that may occur when an individual is anxious. Examples include “I am going to pass out” and “I will have a heart attack”. The BSQ is a 17-item scale that measures an individual’s fear of several bodily sensations, such as heart palpitations, dizziness, feeling short of breath. Both questionnaires are rated on 5-point Likert scales, with scores derived by the average rating to each item (range I-5). The scales have demonstrated good psychometric properties (Chambless et al., 1984). Ss completed several questions regarding their experience of panic attacks and panic symptoms. Wording for the questions was adopted from the ADIS-R (DiNardo & Barlow, 1988). Ss first responded to 2 screening questions regarding the occurrence of spontaneous, uncued panic (“Have you had a time when you felt a sudden rush of intense fear or anxiety or feeling of impending doom?” and “Have you ever had this feeling come either ‘from out of the blue’, or whiie you are at home alone, or in a situation where you did not expect it to occur?“). Ss who answered Yes to both of these questions then checked the symptoms that occur during these attacks from a list of the 13 DSM-IIIR panic attack symptoms. Finally, Ss were asked if they ever had experienced at least 4 of these attacks in a 4-week period; if they ever worried almost every day for at least a month about having another anxiety attack (and if they worried almost every day over the last month); and if, during some of the attacks, at least 4 of these symptoms ever developed suddenly
414
RICHARD
E. CARR et al
and increased in intensity within 10 min or less. Ss also reported how mny unexpected anxiety attacks they experienced in the past month. Pulmonary function. Pulmonary function was assessed by spirometry. Ss forcefully exhaled 3 times from maximal lung capacity, or until at least 2 equivalent readings (+ 5%) were obtained. Measures included forced vital capacity (FVC), forced expiratory volume in 1 set (FEV,), forced expiratory flow at 50% vital capacity (FEFSO), and the ratio of FEV, to FVC (FEV, /FVC). FVC represents the volume of air that a person can exhale forcefully with maximal effort. It is not reliably affected by asthmatic obstruction. FEV, is the volume of air forcefully exhaled within the first second of the test. The ratio FEV,/FVC is inversely related to the degree of airway obstruction. Airflow obstruction reduces flow rates during the first second of forced exhalation, thereby reducing the FEV,/FVC as well as FEFSO. Whereas FEV, is quite effort-dependent, FEFSO is much less so and reflects airflow rates in the middle airways. All measures (except FEV, /FVC) were analyzed as the percent predicted based on the S’s height, weight, age, and gender. Spirometry was taken on a PneuMedics Mega 4000 pneumotachograph spirometer. ClasGjication
of asthmatic
subjects
Panic attacks. Asthmatic Ss were classified as PD if they reported: (A) the occurrence of spontaneous panic attacks (minimum of 4 DSM-IIIR panic symptoms with the attacks); (B) that the symptoms reached peak intensity in < 10 min (‘sudden onset’ criteria); (C) the occurrence of 4 unexpected attacks in any 4-week period; and (D) at least 1 unexpected panic attack in the past month. Anxiety sensitivity. An AS1 score is classified as high if it falls 1 SD above the mean, low if it falls 1 SD below the mean, and medium if it falls between these scores (Donnell & McNally, 1989). In previous studies, high AS1 has been defined as a score of > 30 for women and 323 for men (Reiss et al., 1986); or using normative data for college students, 227 for ‘high’, lo-26 for ‘medium’, and 9 or lower for ‘low’, with no sex differences (Peterson & Reiss, 1987). Since our Ss were asthmatics and were not all college students, it was decided to use the mean and standard deviation of the present sample for classifying the 5’s, rather than norms derived from nonmedical college samples. The mean AS1 score for the total sample of asthmatics was 17.2 (SD = 7.9). Therefore, Ss who scored 225 were classified as high, ~9 as low, and 10-24 as medium anxiety sensitivity. Procedure Ss signed Questionnaires spirometry.
an informed consent statement after a verbal description of the procedures. were completed in random order followed by pulmonary function assessment by
RESULTS
Table 1 lists the S characteristics for the sample of asthma patients. Of the 93 patients with asthma, 21 (22.6%) reported a history of panic attacks with 9 (9.7% of the total asthmatic sample) of the 21 panickers reporting the DSM-IIIR criteria for PD. Asthmatic Ss with PD (AS-PD group)
I set; FEFSO = forced expiratory Row at 50% vital capacity. FVC, FEV,, and FEFSO are expressed as percent predicted based on age. sex, height, and weight.
Panic attacks Table 2. Proportion as a function
and asthma of Ss reporting of ASI force
415 PD
AS1 score
N
PD
High Medium LOW
17 59 17
35.3% (6)’ 5.1% (3) 0.0% (0)
+P < 0.003, Fisher’s exact test.
reported an average of 2.9 panic attacks over the past month (SD = 2.0) and 6.6 symptoms per attack (SD = 1.9). None were currently receiving treatment; however, 2 reported having received some form of psychotherapy and/or medication for panic attacks in the past. The sample also displayed mild airway obstruction, as reflected by a mean FEV,/FVC ratio of 0.71, and a mean FEFSO of 49.7% expected. As is usual among asthmatics, FVC tended to be normal (94.2% expected). Anxiety sensitivity and panic. Seventeen (18.3%) Ss were classified as high AS1 (i.e. 1 SD above the sample mean), 59 Ss (63.4%) were medium, and 17 were low (18.3%). As Table 2 shows, the proportion of Ss reporting PD was significantly related to AS1 classification, P < 0.003, Fisher’s exact test. Among those scoring high on ASI, 35.3% reported PD criteria compared to 5.1% among those classified as medium ASI, and 0% among the 17 with low AS1 scores. Pulmonary function and panic. Two analyses were performed to determine: (1) if pulmonary function was worse among asthmatics with PD than among those without PD; and (2) if the relationship between anxiety sensitivity and PD was mediated by a link between worse pulmonary function and high anxiety sensitivity. First, pulmonary function test results for the 2 groups (asthmatics with and without PD) were subject to multivariate analyses. Wilks’ lambda was nonsignificant. Means for each of the 4 pulmonary function tests-FEV, (83.1% vs 85.3%) FEV, /FVC (0.71 vs 0.70) FVC (94.1% vs 95.4%) and FEFSO (49.4% vs 52.7%)-for the AS (N = 80) vs AS-PD (N = 9) groups, respectively, were nearly identical, suggesting that sample size does not account for the lack of significance. Next, results of the 4 pulmonary function measures were correlated with anxiety sensitivity scores. Anxiety sensitivity was unrelated to any of the pulmonary measures-FVC r(83) = -0.06, FEV, r(83) = 0.03, FEV, /FVC r(83) = 0.13, or FEFSO r(83) = 0.16-thus indicating that the relationship between anxiety sensitivity and PD was not mediated by more impaired pulmonary function. Panic-related cognitions in asthma and PD. A 2 x 2 factorial analysis of variance was performed to determine: (1) if asthma is associated with high ratings of panic-related cognitions independent of the presence of PD, and (2) if asthmatics with PD reported higher ratings of panic-related cognitions than did those without PD. There were 2 levels (absent vs present) for each of the 2 variables, PD and asthma. The 4 groups were: AS (N = 84); AS-PD (N = 9); PD (N = 10); and Nor (N = 32). For the BSQ there was a nonsignificant Asthma x PD interaction, F(1,112) = 3.72, NS. Main effects for Asthma were nonsignificant, F( 1,112) = 0.70, NS, but were highly significant for PD, F( 1,112) = 20.59, P < 0.0001. As Fig. 1 shows, Ss with PD (asthmatics and nonasthmatics) reported similarly high ratings of fear of bodily sensations (AS-PD--M = 2.48, SD = 0.7; PD--M = 2.96, SD = 0.9) relative to Ss without PD (AS-A4 = 2.03, SD = 0.6; Nor-M = 1.84, SD = 0.8). Figure 2 displays the average AS1 scores for the 4 groups. There was a highly significant main effect for PD, F( 1,112) = 39.0, P < 0.0001, and a significant main effect for asthma, F( 1,112) = 5.12, P < 0.03, qualified by a significant Asthma x PD interaction, F( 1,1 12) = 5.28, P < 0.03. AS1 scores are higher for both PD groups (AS-PD--M = 24.9, SD = 4.8; PDA4 = 34.8, SD = 10.7) than for nonpanicking Ss (AS--M = 16.3, SD = 7.8; Nor--M = 16.2, SD = 10.1) but differences are significantly greater among nonasthmatics. As Fig. 2 shows, the main effect for asthma is explained by the much higher AS1 mean score of the nonasthmatic PD patients. Among nonpanickers, the presence of asthma had no effect on AS1 scores (16.3 vs 16.2). More importantly, as with the BSQ, the mean AS1 score for asthmatics with PD (24.9) was significantly higher than that for asthmatics without PD (16.3) t(82) = 2.92, P < 0.005.
RICHARD E. CARR ef al.
416 3.0 -
0 Panic l
No panic
2.5 E H $T 2.0 m ,” 5
l *.
1.5 -
I
1.0
No asthma
Asthma Fig. 1. Mean
BSQ score by group.
Finally, an analysis of catastrophic cognitions (ACQ) revealed a highly significant interaction, F( 1,106) = 16.7, P < 0.0001. Figure 3 displays the mean score for each group (AS-PD--M = 1.63, SD = 0.4; PD--M = 2.46, SD = 0.8; AS--M = 1.44, SD = 0.3; Nor--M = 1.40, SD = 0.4). The small difference between means for asthmatics with PD and asthmatics without PD was not significant, t(77) = 1.3, NS. In summary, Ss with PD-asthmatics and nonasthmatics-displayed more fear of bodily sensations (BSQ) and more negative beliefs about the consequences of anxiety (ASI) relative to those without PD. In addition, the presence of asthma alone had no effect on these measures of panic-related cognitions; only asthmatics with PD had elevated scores. Finally, scores among asthmatics with PD tended to be lower than those among nonasthmatics with PD.
DISCUSSION The purpose of this study was to investigate among asthmatics the relationship between anxiety sensitivity and PD, and to examine the effects of asthma and PD on 3 measures of fear of fear (anxiety sensitivity, fear of body sensations, and catastrophic cognitions). The results suggest the following. First, the experience of severe and frequent panic attacks (i.e. PD) is significantly more common among both asthmatics and nonasthmatics who express negative beliefs about somatic sensations (i.e. high anxiety sensitivity). Among asthmatics classified as high ASI, 35.3% had PD, compared to 5.1% among those classified as medium ASI, and 0% among those with low ASI. Moreover, these results are not due to differences in pulmonary function. Measures of pulmonary function coefficients were equivalent between those with PD vs those without PD, and all correlation
.
.
I
15
No asthma
Asthma Fig. 2. Mean AS1 score by group
Panic attacks 2.50 -
0
Panic
l
No panic
and asthma
417
2.25 2 g
2.00 -
T c
1.75 -
Lz 1.50 -
I
1.25 1
No asthma
Asthma Fig. 3. Mean ACQ score by group.
between AS1 scores and pulmonary function tests were nonsignificant. These results offer strong support for Clark (Clark, 1986; Clark, Salkovskis, Gelder, Koehler, Martin, Anastasiades, Hackman, Middleton & Jeavons, 1988) and Beck’s (1988) cognitive model in which catastrophic misinterpretations of somatic sensations are deemed necessary, but not sufficient, for the development of PD. Second, an analysis of the 3 measures of panic-related cognitions revealed that asthma alone-a disease characterized by frequent (and often severe) bouts of dyspnea, wheezing, and hyperventilation-is not associated with elevated fears of bodily sensations, or with irrational beliefs about the consequences of anxiety, or with catastrophic cognitions. On the other hand, asthma patients with PD displayed significantly higher ratings on these measures relative to asthmatics without PD. Thus, although the incidence of PD is reportedly higher among those with asthma than among the general population (e.g. Yellowlees et al., 1987, 1988), this cannot be explained by the mere presence of an airways disease nor by the degree of pulmonary impairment and its associated symptoms. Rather, the present findings concur with those of Porzelius et al. (1992) in providing evidence that the occurrence of panic attacks among individuals with a respiratory disease (e.g. asthma or COPD) is due to misinterpretations of bodily sensations, as similarly found among the general population (e.g. Clark, 1986; Donnell & McNally, 1990). Although panic symptoms are apparently unrelated to current pulmonary condition, it is possible that the experience of severe pulmonary dysfunction in the past is a relevant factor. Asthma severity varies widely within individuals over time. It is possible that the experience of severe asthma attacks in the past may have sensitized some asthmatic individuals to respiratory sensations, leading to increased anxiety about these sensations; however, the present data do not provide evidence for this possibility. The data on PD among asthmatics-as well as among nonasthmatics-indicate that specific cognitions, such as fear of body sensations, is critical for developing PD. However, the threshold for developing PD may be lower among asthmatics, perhaps because of frightening experiences with dyspnea that many of them may have experienced in the course of their disease. Yellowlees and his colleagues (Yellowlees et al., 1987, 1988) found a particularly high rate of PD among asthmatics, a number of whom had reported ‘near death’ experiences from asthma. Other factors related to asthma may contribute to panic symptoms, even among asthmatics who never experienced such a severe asthma attack. Lehrer, Isenberg and Hochron (1993) hypothesized several additional factors that may predispose asthmatics to panic symptoms. One may be the frequent experience of hyperventilation, which may be related to hyperreactivity of CNS centers controlling respiratory drive. A second may be a reaction to asthma medications. Adrenergic-agonist, theophylline, and steroid medications all have been implicated in provoking anxiety and other negative emotional states (e.g. Milgrom & Bender, 1993). A third may be the negative emotion produced by having a chronic disease. Although the results of this study indicate that none of these factors is, by itself, sufficient to produce PD in asthmatics, these factors may increase
418
RICHARD ECARR
et al
vulnerability to panic. Furthermore, the results show that without the panicogenic cognitions, PD does not occur at all, among either asthmatics or nonasthmatics. The present study is limited by our exclusive reliance on self-reported panic attack history for the asthmatics, and by the absence of an assessment of other factors that may have predisposed asthmatics to experience PD. Nevertheless, given the number of individuals who are at risk of developing PD by virtue of their negative beliefs about the consequences of somatic sensations (high ASI), and the high prevalence of PD in asthma, researchers might fruitfully explore the preventive effects of cognitive restructuring techniques (e.g. Clark, 1989) in this particularly high-risk group. Ack,loM’ledgemenrs-This research was supported by Grants Nos. HL 08789 and HL 44097 from the National Institutes of Health. The authors wish to thank Tammy Fallon for her help in data entry, Barry Wolf, David Goldstein, Martin Sheehy and Matthew Smith for physical examinations of patients, and Peggy Sarno for administrative assistance.
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R. A. & Heibronner, of Anvieiy
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1994 Copyright cc 1994 Elsevier Science Ltd Printed in Great Britain. All rights reserved 0005-7967/94 $6.00 + 0.00
Pergamon
ANXIETY
SENSITIVITY AND PANIC ATTACKS ASTHMATIC POPULATION
RICHARD
E. CARR,
PAUL
M.
STUART Department
of psychiatry,
Robert
LEHRER,* M.
LAWRENCE
IN AN
L. RAUSCH
and
UMDNJ,
Piscataway,
HOCHRON
Wood Johnson Medical NJ 08854-5635, U.S.A.
School,
(Received 10 March 1993) Summary-The purpose of this study was to examine the relationship among anxiety sensitivity, the experience of frequent, spontaneous panic attacks, and pulmonary function in individuals with asthma. Ninety-three asthmatics participated by completing a battery of questionnaires and a spirometric assessment. Twenty-three percent of the asthmatics reported a history of spontaneous panic attacks with 9.7% reporting attacks that were severe and frequent enough to meet the DSM-IIIR criteria for panic disorder (PD). Anxiety sensitivity (ASI) scores, but not pulmonary function, was significantly related to PD. In addition, we compared the asthmatics (with and without PD) to 10 clinically diagnosed PD Ss without asthma and to 32 nonanxious, nonasthmatic controls on the ASI, the Body Sensations Questionnaire. and the Agoraphobic Cognitions Questionnaire. Whereas Ss with PD (asthmatic and nonasthmatic) displayed significant elevations on these measures compared to those without PD, the presence of asthma alone had no effect. The present study concurs with that of Porzelius et al. [BehaGur Research and Therapy, 30, 75-77 (1992)] in extending the validity of the cognitive model of PD to individuals with pulmonary disease.
INTRODUCTION
The study of asthma can be an important source for understanding the relative contributions of respiratory abnormalities and of cognitions to panic-related experiences (Carr, Lehrer & Hochron, 1992; Porzelius, Vest & Nochomovitz, 1992; Yellowlees, Alpers, Bowden, Bryant & Ruffin, 1987; Yellowlees, Haynes, Potts & Ruffin, 1988; Kinsman, Luparello, O’Banion & Spector, 1973). Asthma is a respiratory disease characterized by hyperreactive airways. The symptoms include wheezing and congestion, as well as hyperventilation (e.g. dyspnea, dizziness, racing heart), the last of which is common also to panic disorder (PD). Moreover, the catastrophic misinterpretation of physical sensations, particularly hyperventilation-induced sensations, is central to cognitive theories regarding the genesis and maintenance of PD (Clark, 1986; Beck, 1988). The experience of hyperventilation-induced dyspnea is also central to Ley’s dyspnea-fear theory of PD (Ley, 1989). In addition to sharing a number of physical symptoms, PD and asthma show a high incidence of comorbidity. For example, Kinsman et al. (1973) found that 42% of asthmatics reported that panic-fear occurred frequently with their asthma attacks. Yellowlees et al. (1987) found a high rate of anxiety disorders (34%) among a sample of 50 asthmatics in Australia, 12 (24%) of whom received a diagnosis of PD. In a follow-up study, approximately 12% of 49 asthmatic subjects (Ss) met the DSM-III (APA, 1980) criteria for PD as assessed by structured interview (Yellowlees et al., 1988). Whereas these studies document a higher than normal rate of panic among those with asthma, others have tried to explain it by searching for possible differences in pulmonary function or in cognitions between asthmatics with PD vs those without PD. For example, Porzelius et al. (1992) reported that 37% of a sample of 48 patients with chronic obstructive pulmonary disease (COPD) experienced panic attacks. Interestingly, although panickers did not differ from nonpanickers in either severity of their pulmonary disease or severity of shortness of breath, they were distinguished by more frequent agoraphobic cognitions and greater fear of body sensations. The data suggest *To whom
all reprint
requests
should
be addressed. 411
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that COPD patients experience panic attacks because the symptoms are misinterpreted, not because of high generalized anxiety, depression, or more severe pulmonary impairment. By contrast, a previous study in this laboratory (Carr et al., 1992) found that panic-fear among asthmatics, but not among ADIS-R-diagnosed [Anxiety Disorders Interview Schedule-Revised (DiNardo & Barlow, 1988)] PD patients, was strongly related to severity ratings of dyspnea. These results suggest that dyspnea plays a more central role in the experience of panic-fear among asthmatics than it does among nonasthmatic PD patients. Despite interest in studying the interaction between respiratory symptoms and catastrophic cognitions among Ss with varying degrees of pulmonary disease, research in this area has lacked a critical measure of psychological vulnerability to panic-related phenomena: anxiety sensitivity. Anxiety sensitivity reflects an individual’s concerns about the consequences of experiencing anxiety-related symptoms. It is described by Reiss & McNally (1985) as a personality trait that increases an individual’s conditionability for fear [see Reiss (1991) for a review]. It is highly stable over time (Maller & Reiss, 1992) distinct from state and trait anxiety (Reiss, 1991) and better able to predict panic attack frequency and a history of PD than is generalized or trait anxiety (Reiss, Peterson, Gursky & McNally, 1986). In a study of 425 college students, Donnell & McNally (1990) found a significantly higher proportion of Ss reporting spontaneous panic attacks among those classified as high (32.4%) on the Anxiety Sensitivity Index (ASI) than among those classified as medium (15.6%) or low (5.1%). High AS1 Ss also reported more frequent treatment-seeking and a greater first-degree family history of panic than did others. In addition, high anxiety sensitivity has been shown to predict affective response to CO, inhalation better than Hamilton Anxiety scores, social anxiety, and depression (Rapee, Brown, Antony & Barlow, 1992); and, in one study of hyperventilation challenge, high anxiety sensitivity was a better predictor of response than was a history of panic attacks (Holloway & McNally, 1987; Donnell & McNally, 1989). Finally, since two-thirds of Ss with high anxiety sensitivity have never experienced a panic attack, prior experience of panic is not a necessary causal factor either of high anxiety sensitivity or of exaggerated reactions to biological challenges (Donnell & McNally, 1990). Reiss et al. (1986) conclude that in order to predict panic, it is more valuable to know what an individual expects to happen as a result of becoming anxious than it is to know how frequently they experience anxiety symptoms. This may explain the high rate of panic attacks and specifically PD among asthmatics. Asthmatics experience more symptoms of dyspnea and hyperventilation than do nonasthmatics, and sometimes these symptoms can be associated with life-threatening asthma exacerbations; however, not all asthmatics experience panic. Thus, panic attacks in this population may depend more on concerns about these sensations (i.e. anxiety sensitivity) than on the actual severity of the illness (i.e. objective measures of pulmonary function). Therefore, PD among persons with asthma should show a relationship to anxiety sensitivity that is similar to that previously found among nonasthmatics (e.g. Donnell & McNally, 1990); and asthmatics with PD should also show elevated scores on measures of catastrophic cognitions and fear of body sensations, relative to those without PD. The purpose of this study was twofold. First, to determine if a relationship exists between anxiety sensitivity and PD among persons with asthma. Second, to compare measures of panic-related cognitions among 4 groups: (1) asthma Ss without PD (AS); (2) asthma Ss who report the DSM-IIIR criteria for PD (AS-PD); (3) nonasthmatic, nonpanicking control Ss (Nor); and (4) PD patients who do not have asthma (PD). The study specifically addresses the following 4 questions: (1) Does the proportion of asthmatics who have PD increase as a function of anxiety sensitivity? (2) Do asthmatics with PD suffer from worse pulmonary function relative to asthmatics without PD? (3) Do asthmatics with PD report high ratings of panic-related cognitions than do those without PD? (4) Is asthma associated with high ratings of panic-related cognitions independent of the presence of PD?
Panic attacks and asthma
413
METHOD
A total of 13.5Ss participated in the study. The asthmatic sample consisted of 93 Ss (51 females) recruited via newspaper and radio advertisements, posted announcements, and physician referrals. They had an average age of 25.9 years (SD = 6.6). Diagnoses of asthma were made by a board-certified pulmonary physician on the basis of history, physical examination, spirometry, bronchodilator response to albuterol, and a diffusing capacity test. They were also screened to rule out medical diseases other than asthma. Thirty-two nonasthmatics (Nor group, 19 females) with an average age of 29.1 years (SD = ?.l), and who were screened to rule out a history of panic attacks or other psychiatric problems, were similarly recruited via posted announcements and newspaper advertisements. Finally, 10 nonasthmatic patients (PD group, 7 females) with a diagnosis of PD and an average age of 33.0 years (SD = 6.0) were recruited from physician referrals and newspaper advertisements. Diagnoses of PD according to DSM-IIIR criteria (APA, 1987) were confirmed by the ADIS-R (DiNardo & Barlow, 1988). Seven of the 10 PD patients were currently undergoing some form of mental health treatment. Three were receiving medication only, 3 were receiving a combination of medication and behavior therapy, and 1 was undergoing behavior therapy only. However, patients were included only if symptomatic during the previous month, as defined by significant daily worry about the occurrence of a panic attack, or report of at least 1 panic attack. Number of years since onset of PD ranged from 1 to 23 years. Excluding the patient with a 23-year history, the average number of years since first panic attack was 8.2. The group reported an average of 4.8 (SD = 3.8) panic attacks over the previous month with an average of 8.8 (SD = 2.0) symptoms per attack. Smokers were excluded from all groups, and nonasthmatic Ss were screened for abnormal pulmonary function. Dependent measwe~ Self-report. Patients completed a battery of questionnaires that included the Anxiety Sensitivity Index (ASI), the Agoraphobic Cognitions Questionnaire (ACQ), and the Body Sensations Questionnaire (BSQ). The AS1 is a valid and reliable l6-item questionnaire measuring an individual’s concerns about the consequences of experiencing anxiety symptoms (e.g. “It scares me when I become short of breath”, “When I notice my heart beating rapidly I worry that I may have a heart attack”). Items are rated on a 0- to 4-point Likert scale, with total scores ranging from 0 to 64 (Peterson & Reiss, 1987; Peterson & Heilbronner, 1987; Reiss et al., 1986; Foa, Steketee & Young, 1984). The ACQ and SSQ are companion scales developed by Chambless (Chambless, Caputo, Bright & Gallagher, 1984) for measuring the construct of fear of fear. The ACQ is a 1Citem scale assessing the presence of specific catastrophic thoughts that may occur when an individual is anxious. Examples include “I am going to pass out” and “I will have a heart attack”. The BSQ is a 17-item scale that measures an individual’s fear of several bodily sensations, such as heart palpitations, dizziness, feeling short of breath. Both questionnaires are rated on 5-point Likert scales, with scores derived by the average rating to each item (range I-5). The scales have demonstrated good psychometric properties (Chambless et al., 1984). Ss completed several questions regarding their experience of panic attacks and panic symptoms. Wording for the questions was adopted from the ADIS-R (DiNardo & Barlow, 1988). Ss first responded to 2 screening questions regarding the occurrence of spontaneous, uncued panic (“Have you had a time when you felt a sudden rush of intense fear or anxiety or feeling of impending doom?” and “Have you ever had this feeling come either ‘from out of the blue’, or whiie you are at home alone, or in a situation where you did not expect it to occur?“). Ss who answered Yes to both of these questions then checked the symptoms that occur during these attacks from a list of the 13 DSM-IIIR panic attack symptoms. Finally, Ss were asked if they ever had experienced at least 4 of these attacks in a 4-week period; if they ever worried almost every day for at least a month about having another anxiety attack (and if they worried almost every day over the last month); and if, during some of the attacks, at least 4 of these symptoms ever developed suddenly
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and increased in intensity within 10 min or less. Ss also reported how mny unexpected anxiety attacks they experienced in the past month. Pulmonary function. Pulmonary function was assessed by spirometry. Ss forcefully exhaled 3 times from maximal lung capacity, or until at least 2 equivalent readings (+ 5%) were obtained. Measures included forced vital capacity (FVC), forced expiratory volume in 1 set (FEV,), forced expiratory flow at 50% vital capacity (FEFSO), and the ratio of FEV, to FVC (FEV, /FVC). FVC represents the volume of air that a person can exhale forcefully with maximal effort. It is not reliably affected by asthmatic obstruction. FEV, is the volume of air forcefully exhaled within the first second of the test. The ratio FEV,/FVC is inversely related to the degree of airway obstruction. Airflow obstruction reduces flow rates during the first second of forced exhalation, thereby reducing the FEV,/FVC as well as FEFSO. Whereas FEV, is quite effort-dependent, FEFSO is much less so and reflects airflow rates in the middle airways. All measures (except FEV, /FVC) were analyzed as the percent predicted based on the S’s height, weight, age, and gender. Spirometry was taken on a PneuMedics Mega 4000 pneumotachograph spirometer. ClasGjication
of asthmatic
subjects
Panic attacks. Asthmatic Ss were classified as PD if they reported: (A) the occurrence of spontaneous panic attacks (minimum of 4 DSM-IIIR panic symptoms with the attacks); (B) that the symptoms reached peak intensity in < 10 min (‘sudden onset’ criteria); (C) the occurrence of 4 unexpected attacks in any 4-week period; and (D) at least 1 unexpected panic attack in the past month. Anxiety sensitivity. An AS1 score is classified as high if it falls 1 SD above the mean, low if it falls 1 SD below the mean, and medium if it falls between these scores (Donnell & McNally, 1989). In previous studies, high AS1 has been defined as a score of > 30 for women and 323 for men (Reiss et al., 1986); or using normative data for college students, 227 for ‘high’, lo-26 for ‘medium’, and 9 or lower for ‘low’, with no sex differences (Peterson & Reiss, 1987). Since our Ss were asthmatics and were not all college students, it was decided to use the mean and standard deviation of the present sample for classifying the 5’s, rather than norms derived from nonmedical college samples. The mean AS1 score for the total sample of asthmatics was 17.2 (SD = 7.9). Therefore, Ss who scored 225 were classified as high, ~9 as low, and 10-24 as medium anxiety sensitivity. Procedure Ss signed Questionnaires spirometry.
an informed consent statement after a verbal description of the procedures. were completed in random order followed by pulmonary function assessment by
RESULTS
Table 1 lists the S characteristics for the sample of asthma patients. Of the 93 patients with asthma, 21 (22.6%) reported a history of panic attacks with 9 (9.7% of the total asthmatic sample) of the 21 panickers reporting the DSM-IIIR criteria for PD. Asthmatic Ss with PD (AS-PD group)
I set; FEFSO = forced expiratory Row at 50% vital capacity. FVC, FEV,, and FEFSO are expressed as percent predicted based on age. sex, height, and weight.
Panic attacks Table 2. Proportion as a function
and asthma of Ss reporting of ASI force
415 PD
AS1 score
N
PD
High Medium LOW
17 59 17
35.3% (6)’ 5.1% (3) 0.0% (0)
+P < 0.003, Fisher’s exact test.
reported an average of 2.9 panic attacks over the past month (SD = 2.0) and 6.6 symptoms per attack (SD = 1.9). None were currently receiving treatment; however, 2 reported having received some form of psychotherapy and/or medication for panic attacks in the past. The sample also displayed mild airway obstruction, as reflected by a mean FEV,/FVC ratio of 0.71, and a mean FEFSO of 49.7% expected. As is usual among asthmatics, FVC tended to be normal (94.2% expected). Anxiety sensitivity and panic. Seventeen (18.3%) Ss were classified as high AS1 (i.e. 1 SD above the sample mean), 59 Ss (63.4%) were medium, and 17 were low (18.3%). As Table 2 shows, the proportion of Ss reporting PD was significantly related to AS1 classification, P < 0.003, Fisher’s exact test. Among those scoring high on ASI, 35.3% reported PD criteria compared to 5.1% among those classified as medium ASI, and 0% among the 17 with low AS1 scores. Pulmonary function and panic. Two analyses were performed to determine: (1) if pulmonary function was worse among asthmatics with PD than among those without PD; and (2) if the relationship between anxiety sensitivity and PD was mediated by a link between worse pulmonary function and high anxiety sensitivity. First, pulmonary function test results for the 2 groups (asthmatics with and without PD) were subject to multivariate analyses. Wilks’ lambda was nonsignificant. Means for each of the 4 pulmonary function tests-FEV, (83.1% vs 85.3%) FEV, /FVC (0.71 vs 0.70) FVC (94.1% vs 95.4%) and FEFSO (49.4% vs 52.7%)-for the AS (N = 80) vs AS-PD (N = 9) groups, respectively, were nearly identical, suggesting that sample size does not account for the lack of significance. Next, results of the 4 pulmonary function measures were correlated with anxiety sensitivity scores. Anxiety sensitivity was unrelated to any of the pulmonary measures-FVC r(83) = -0.06, FEV, r(83) = 0.03, FEV, /FVC r(83) = 0.13, or FEFSO r(83) = 0.16-thus indicating that the relationship between anxiety sensitivity and PD was not mediated by more impaired pulmonary function. Panic-related cognitions in asthma and PD. A 2 x 2 factorial analysis of variance was performed to determine: (1) if asthma is associated with high ratings of panic-related cognitions independent of the presence of PD, and (2) if asthmatics with PD reported higher ratings of panic-related cognitions than did those without PD. There were 2 levels (absent vs present) for each of the 2 variables, PD and asthma. The 4 groups were: AS (N = 84); AS-PD (N = 9); PD (N = 10); and Nor (N = 32). For the BSQ there was a nonsignificant Asthma x PD interaction, F(1,112) = 3.72, NS. Main effects for Asthma were nonsignificant, F( 1,112) = 0.70, NS, but were highly significant for PD, F( 1,112) = 20.59, P < 0.0001. As Fig. 1 shows, Ss with PD (asthmatics and nonasthmatics) reported similarly high ratings of fear of bodily sensations (AS-PD--M = 2.48, SD = 0.7; PD--M = 2.96, SD = 0.9) relative to Ss without PD (AS-A4 = 2.03, SD = 0.6; Nor-M = 1.84, SD = 0.8). Figure 2 displays the average AS1 scores for the 4 groups. There was a highly significant main effect for PD, F( 1,112) = 39.0, P < 0.0001, and a significant main effect for asthma, F( 1,112) = 5.12, P < 0.03, qualified by a significant Asthma x PD interaction, F( 1,1 12) = 5.28, P < 0.03. AS1 scores are higher for both PD groups (AS-PD--M = 24.9, SD = 4.8; PDA4 = 34.8, SD = 10.7) than for nonpanicking Ss (AS--M = 16.3, SD = 7.8; Nor--M = 16.2, SD = 10.1) but differences are significantly greater among nonasthmatics. As Fig. 2 shows, the main effect for asthma is explained by the much higher AS1 mean score of the nonasthmatic PD patients. Among nonpanickers, the presence of asthma had no effect on AS1 scores (16.3 vs 16.2). More importantly, as with the BSQ, the mean AS1 score for asthmatics with PD (24.9) was significantly higher than that for asthmatics without PD (16.3) t(82) = 2.92, P < 0.005.
RICHARD E. CARR ef al.
416 3.0 -
0 Panic l
No panic
2.5 E H $T 2.0 m ,” 5
l *.
1.5 -
I
1.0
No asthma
Asthma Fig. 1. Mean
BSQ score by group.
Finally, an analysis of catastrophic cognitions (ACQ) revealed a highly significant interaction, F( 1,106) = 16.7, P < 0.0001. Figure 3 displays the mean score for each group (AS-PD--M = 1.63, SD = 0.4; PD--M = 2.46, SD = 0.8; AS--M = 1.44, SD = 0.3; Nor--M = 1.40, SD = 0.4). The small difference between means for asthmatics with PD and asthmatics without PD was not significant, t(77) = 1.3, NS. In summary, Ss with PD-asthmatics and nonasthmatics-displayed more fear of bodily sensations (BSQ) and more negative beliefs about the consequences of anxiety (ASI) relative to those without PD. In addition, the presence of asthma alone had no effect on these measures of panic-related cognitions; only asthmatics with PD had elevated scores. Finally, scores among asthmatics with PD tended to be lower than those among nonasthmatics with PD.
DISCUSSION The purpose of this study was to investigate among asthmatics the relationship between anxiety sensitivity and PD, and to examine the effects of asthma and PD on 3 measures of fear of fear (anxiety sensitivity, fear of body sensations, and catastrophic cognitions). The results suggest the following. First, the experience of severe and frequent panic attacks (i.e. PD) is significantly more common among both asthmatics and nonasthmatics who express negative beliefs about somatic sensations (i.e. high anxiety sensitivity). Among asthmatics classified as high ASI, 35.3% had PD, compared to 5.1% among those classified as medium ASI, and 0% among those with low ASI. Moreover, these results are not due to differences in pulmonary function. Measures of pulmonary function coefficients were equivalent between those with PD vs those without PD, and all correlation
.
.
I
15
No asthma
Asthma Fig. 2. Mean AS1 score by group
Panic attacks 2.50 -
0
Panic
l
No panic
and asthma
417
2.25 2 g
2.00 -
T c
1.75 -
Lz 1.50 -
I
1.25 1
No asthma
Asthma Fig. 3. Mean ACQ score by group.
between AS1 scores and pulmonary function tests were nonsignificant. These results offer strong support for Clark (Clark, 1986; Clark, Salkovskis, Gelder, Koehler, Martin, Anastasiades, Hackman, Middleton & Jeavons, 1988) and Beck’s (1988) cognitive model in which catastrophic misinterpretations of somatic sensations are deemed necessary, but not sufficient, for the development of PD. Second, an analysis of the 3 measures of panic-related cognitions revealed that asthma alone-a disease characterized by frequent (and often severe) bouts of dyspnea, wheezing, and hyperventilation-is not associated with elevated fears of bodily sensations, or with irrational beliefs about the consequences of anxiety, or with catastrophic cognitions. On the other hand, asthma patients with PD displayed significantly higher ratings on these measures relative to asthmatics without PD. Thus, although the incidence of PD is reportedly higher among those with asthma than among the general population (e.g. Yellowlees et al., 1987, 1988), this cannot be explained by the mere presence of an airways disease nor by the degree of pulmonary impairment and its associated symptoms. Rather, the present findings concur with those of Porzelius et al. (1992) in providing evidence that the occurrence of panic attacks among individuals with a respiratory disease (e.g. asthma or COPD) is due to misinterpretations of bodily sensations, as similarly found among the general population (e.g. Clark, 1986; Donnell & McNally, 1990). Although panic symptoms are apparently unrelated to current pulmonary condition, it is possible that the experience of severe pulmonary dysfunction in the past is a relevant factor. Asthma severity varies widely within individuals over time. It is possible that the experience of severe asthma attacks in the past may have sensitized some asthmatic individuals to respiratory sensations, leading to increased anxiety about these sensations; however, the present data do not provide evidence for this possibility. The data on PD among asthmatics-as well as among nonasthmatics-indicate that specific cognitions, such as fear of body sensations, is critical for developing PD. However, the threshold for developing PD may be lower among asthmatics, perhaps because of frightening experiences with dyspnea that many of them may have experienced in the course of their disease. Yellowlees and his colleagues (Yellowlees et al., 1987, 1988) found a particularly high rate of PD among asthmatics, a number of whom had reported ‘near death’ experiences from asthma. Other factors related to asthma may contribute to panic symptoms, even among asthmatics who never experienced such a severe asthma attack. Lehrer, Isenberg and Hochron (1993) hypothesized several additional factors that may predispose asthmatics to panic symptoms. One may be the frequent experience of hyperventilation, which may be related to hyperreactivity of CNS centers controlling respiratory drive. A second may be a reaction to asthma medications. Adrenergic-agonist, theophylline, and steroid medications all have been implicated in provoking anxiety and other negative emotional states (e.g. Milgrom & Bender, 1993). A third may be the negative emotion produced by having a chronic disease. Although the results of this study indicate that none of these factors is, by itself, sufficient to produce PD in asthmatics, these factors may increase
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vulnerability to panic. Furthermore, the results show that without the panicogenic cognitions, PD does not occur at all, among either asthmatics or nonasthmatics. The present study is limited by our exclusive reliance on self-reported panic attack history for the asthmatics, and by the absence of an assessment of other factors that may have predisposed asthmatics to experience PD. Nevertheless, given the number of individuals who are at risk of developing PD by virtue of their negative beliefs about the consequences of somatic sensations (high ASI), and the high prevalence of PD in asthma, researchers might fruitfully explore the preventive effects of cognitive restructuring techniques (e.g. Clark, 1989) in this particularly high-risk group. Ack,loM’ledgemenrs-This research was supported by Grants Nos. HL 08789 and HL 44097 from the National Institutes of Health. The authors wish to thank Tammy Fallon for her help in data entry, Barry Wolf, David Goldstein, Martin Sheehy and Matthew Smith for physical examinations of patients, and Peggy Sarno for administrative assistance.
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