BEHAVIOR THERAPY 27, 115-126, 1996

Suffocation False Alarms and Efficacy of Cognitive Behavioral Therapy

for Panic Disorder

STEVEN TAYLOR

SHEILA WOODY

WILLIAM J. KOCh

PETER D. MCLEAN

KENT W. ANDERSON

University of British Columbia

Cognitive behavioral therapy (CBT) is an effective treatment for many but not all patients with panic disorder. This raises the question of whether there are types of panic disorder for which CBT is effective, and other types for which it is ineffective. Klein's (1993) suffocation alarm theory suggests two types of panic disordered patient: those with intense dyspnea as a frequent panic symptom (suffocation panickers) and those with little or no dyspnea (nonsuffocation panickers). Klein's theory suggests CBT will be less effective for suffocation panickers compared to nonsuffocation panickers. To test this prediction, 22 unmedicated panic-disordered patients were classified as suffocation panickers (n = 13) or nonsuffocation panickers (n = 9) and received 10 sessions of CBT. Both groups had significant reductions in symptoms from pre- to posttreatment, and gains were maintained at 3-month followup. Groups did not differ in treatment response. At 3-month followup 75% of suffocation pan- ickers, and 50% of nonsuffocation panickers were panic-free, and 75% of suffocation panickers and 63% of nonsuffocation panickers were classified as treatment responders. These results fail to support the prediction from Klein's theory and suggest that panic disorder with intense dyspnea can be successfully treated with CBT.

This research was supported by grant M74-90 from the British Columbia Health Research Foundation. We express our thanks to the therapists and other project staff who contributed to this study: Sharon Agar, Bradley Barris, Lisa Brown, Karen Cocco, David Eveleigh, Nichole Fairbrother, Joseph Lenz, Renee Patenaude, Dionne Laslo, Karen Lawson, Randy Paterson, Charlotte Ryan, Zal Saper, and Colin van Uchelen. Sheila Woody is now at the Department of Psychology, Yale University. We thank Dr. S. Rachman for providing helpful comments on an earlier draft of this article.

Correspondence concerning this article should be addressed to Steven Taylor, Department of Psychiatry, University of British Columbia, Vancouver, B.C., Canada, V6T2A1.

115 0005-7894/96/0115-012651.00/0 Copyright 1996 by Association for Advancement of Behavior Therapy

All rights of reproduction in any form reserved.

116 TAYLOR ET AL.

Panic disorder is characterized by recurrent unexpected panic attacks and persistent fear of having further attacks (American Psychiatric Association [APA], 1994). Panic attacks are discrete episodes of intense fear or discomfort associated with symptoms such as dyspnea, palpitations, and fears of dying, going crazy, or losing control (APA). Panic attacks can be regarded as intense psychophysiological alarm reactions, motivating the person to flee potential danger. Panic disorder may arise when the alarm mechanism(s) become hyper- sensitive, firing when there is little or no real danger (i.e., false alarms: Barlow, 1988). These alarms may be due to psychological mechanisms and/or simple physiological detectors (e.g., detectors of central CO2 or lactate levels: Klein, 1993, 1994).

An important psychological component in producing false alarms (and hence panic attacks) may be the tendency to catastrophically misinterpret benign, arousal-related bodily sensations. According to Clark (1986), people with panic disorder have an enduring tendency to misinterpret and overestimate the dan- gerousness of such sensations; e.g., misinterpreting mild humidity-induced breathlessness as a sign of impending suffocation, or misinterpreting palpi- tations as evidence of an impending heart attack. When such sensations are experienced and misinterpreted, the individual becomes anxiously aroused, which increases the intensity of the sensations. Thus, a vicious cycle develops, culminating in a panic attack.

Available evidence provides encouraging support for the role of catastrophic misinterpretation in panic disorder (for reviews, see McNally, 1994; Taylor, 1995). However, an unresolved question concerns the relative importance of cognitive factors and simple physiological alarm mechanisms. There may be several types of panic disorder, arising from dysfunctions in different alarm systems (McNally). Some systems may be defined primarily in terms of cog- nitive mechanisms, whereas others may be defined primarily in terms of simple physiological detectors.

Clark's theory and similar approaches have led to the development of cog- nitive behavioral treatment (CBT) for panic. Studies by Barlow and colleagues (e.g., Barlow, Craske, Cerny, & Klosko, 1989) and by Clark et al. (1994) found that 85 to 90% of patients were panic-free after a course of CBT. How- ever, two recent studies reported lower efficacy, with 25 to 66% of patients panic-free by the end of treatment (Black, Wesner, Bowers, & Gabel, 1993; Shear, Pilkonis, Cloitre, & Leon, 1994). Regardless of the reasons for the differences across studies, the results show that CBT is not effective for all patients with panic disorder. This raises the question of whether CBT is more effective for some types of panic disorder than for others. The purpose of the present study was to determine the efficacy of CBT for the types of panic disorder suggested by Klein's (1993, 1994) suffocation false-alarm theory.

Klein (1993) proposed that "many spontaneous panics occur when the brain's suffocation monitor erroneously signals a lack of useful air, thereby maladap- tively triggering an evolved suffocation alarm system" (p. 306). Alarm acti- vation produces sudden respiratory distress, panic, briefhyperventilation, and

COGNITIVE BEHAVIORAL THERAPY FOR PANIC DISORDER 117

the urge to flee. Unexpected panic attacks occur when the suffocation alarm has a pathologically low threshold for activation, causing it to misfire in a seemingly unpredictable manner. Suffocation false alarms can vary in inten- sity, ranging from limited symptom panics (including isolated episodes of breathlessness) to full-blown panic attacks. Klein suggested that the threshold for alarm activation can be raised by pharmacological treatments, such as imipramine.

Unlike Clark's (1986) cognitive theory of panic, which emphasizes the im- portance of catastrophic misinterpretations, Klein's (1993, 1994) theory mini- mizes the role of psychological factors. The theory is "physiocentric" in that it "makes a deranged physiological control system central to a broad range of symptomatic precipitants and manifestations" (Klein, 1994, p. 506). Klein (1993) conceded that suffocation false alarms can be triggered by psychosocial suffocation cues, which serve as reflex-like releasing stimuli: 'A no-exit situa- tion or one where stuffy, stale air implies no exit, where there are crowded, immobilized people or someone appears to be smothering, might all elicit panic if the suffocation alarm threshold is pathologically lowered or if the cues are particularly salient" (p. 306).

Klein (1993) distinguished suffocation panics (arising from a deranged suffo- cation alarm system) from milder, fear-like panics (which may arise from some other mechanism such as maladaptive learning). In the present study, we refer to panic-disordered patients with deranged suffocation monitors as suffoca- tionpanickers. The other type of patient we will call nonsuffocationpanickers. We classified patients rather than panic attacks because the suffocation alarm theory proposes that people prone to suffocation panics have a trait consisting of a hypersensitive suffocation monitor. We used the theoretically neutral term nonsuffocation panickers instead of fear-like panickers, because the latter im- plies that fear is different from panic (Klein, 1993). This is a contentious dis- tinction that has been challenged by some theorists (e.g., Barlow, 1988).

Klein (1993) cited a good deal of support for his theory, although much of it was circumstantial. Recent studies provide somewhat stronger support. We tested the assumption that hypersensitivity of the suffocation monitor is a risk factor for panic attacks (Taylor & Rachman, 1994). We reasoned that people with hypersensitive suffocation monitors are likely to have histories of alarm activation, and therefore likely to acquire intense fear of suffocation. People with less sensitive monitors are likely to have fewer experiences of alarm activation, and so would be less likely to acquire intense fear of suffocation. Thus, a measure of suffocation fear should provide an indicator of the sen- sitivity of the suffocation monitor. To test this assumption, we administered a newly developed suffocation fear scale (Rachman & Taylor, 1993) to a sample of university students. People scoring high on the scale (n = 49), compared with those scoring low (n = 68), were more likely to panic during a suffo- cation challenge (breathing through a narrow straw for 2 min). This supported the validity of our scale as an index of the sensitivity of the suffocation alarm monitor. In support of Klein's theory, people scoring high on the scale, com-

118 TAYLOR ET AL.

pared with those scoring low, reported a greater lifetime incidence of naturally occurring panic attacks in enclosed spaces (59% vs. 16%) and in other sit- uations (57% vs. 21%), and a greater incidence of unexpected panic attacks (33% vs. 4%).

A recent study by Briggs, Stretch, and Brandon (1993) provides support for the distinction between suffocation panickers and nonsuffocation panickers. Briggs et al. found that people with panic disorder could be divided into two groups, based on the presence or absence of respiratory symptoms during their panic attacks. People with prominent respiratory distress (suffocation panickers), compared with people without these symptoms (nonsuffocation panickers), tended to have more frequent spontaneous panic attacks and fewer situational (cued) attacks. Suffocation panickers, compared to nonsuffocation panickers, also had a better therapeutic response to imipramine, and a poorer response to alprazolam.

A question of clinical significance is whether CBT is equally effective for suffocation panickers and nonsuffocation panickers. Klein's (1993, 1994) theory, with its physiocentric emphasis, suggests that CBT will be less effective for suffocation panickers than for nonsuffocation panickers. It may be that CBT is contraindicated for suffocation panickers, especially if their panics are largely due to a deranged physiological suffocation monitor. On the other hand, Klein's (1993, 1994) theory may underestimate the importance of psychological factors (Taylor & Rachman, 1994), and CBT may be equally effective for suffocation panickers and nonsuffocation panickers. We investigated these possibilities in the present study.

Method Participants

Twenty-two unmedicated patients who met DSM-III-R (and DSM-IV) cri- teria for panic disorder (APA, 1987, 1994) were recruited from family physi- cians and from advertisements in local newspapers and radio. Patients were excluded if they currently met DSM-III-R criteria for any other Axis I dis- order (as assessed by the ADIS-R) or if they were under 18 years of age. Patients also were excluded if they were receiving concurrent psychological treatment elsewhere.

The mean duration of panic disorder was 5 years and most (86%) patients met DSM-III-R (and DSM-IV) criteria for agoraphobia. The sample was 71% female and 81% Caucasian, with a mean age of 34 years (SD = 9 years). With regard to marital status, 57% were married or cohabitating, and the re- mainder were single, divorced, or widowed. Thirteen patients were classified as suffocation panickers, and 9 were classified as nonsuffocation panickers (see below for classification procedures).

Our 22 unmedicated panickers were recruited as part of a study of the re- lationship between panic disorder and major depression (McLean, Woody, Taylor, & Koch, in preparation). The latter study also included 28 panic dis-

COGNITIVE BEHAVIORAL THERAPY FOR PANIC DISORDER 119

ordered patients on psychotropic medication, 17 medicated patients with panic disorder and major depression, and 17 unmedicated patients with panic dis- order and major depression. Patients with major depression were not included in the present study because they received a different treatment protocol than those of the panic-only patients (i.e., 10 sessions of CBT for panic followed by 10 sessions of CBT for depression). Medicated panic-disordered patients (without major depression) were not included in the present study because (1) medication effects may confound the assessment of panic type, and (2) we did not assess whether patients kept their medications constant during the course of CBT. The 22 unmedicated patients included in the present study, compared to the 28 medicated panic-only patients, did not differ in terms of pretreatment severity, ps > .05, as assessed by the seven outcome variables listed in Table 2.

The patients in the present study also were similar to samples used in sev- eral other CBT trials with regard to demographics, panic frequency, propor- tion of agoraphobics (Barlow et al., 1989; Black et al., 1993; Clark et al., 1994; Klosko et al., 1990; Shear et al., 1991, 1994), scores on the Beck Anxiety Inventory (Clark et al.), and scores on the Anxiety Sensitivity Index (Shear et al., 1994).

Measures

Patients were diagnosed with the revised version of the Anxiety Disorders Interview Schedule (ADIS-R: DiNardo & Barlow, 1988). The ADIS-R was used to obtain ratings of symptom severity for each patient's most recent panic and most severe panic. Intensity of each panic symptom was rated on a 0 to 4 scale, ranging from 0 (absent) to 4 (very severe). The ADIS-R also was used to assess the number of full panic attacks over the previous month and the degree of fear of having further attacks. The latter was assessed by a 9-point scale, ranging from 0 (no worry/no fear) to 8 (constantly worried/extreme fear).

Agoraphobic avoidance was assessed by two measures. The first was taken from the agoraphobia module of the ADIS-R, in which the interviewer as- sessed the extent to which the patient avoided each of 19 situations (e.g., driving, shopping malls). Each item was rated on a 5-point scale, ranging from 0 (no avoidance or escape) to 4 (very severe: never enters even with a safe person). Severity of agoraphobic avoidance was measured by the sum of avoidance scores for all 19 situations. Our second measure of agoraphobic avoidance was the Mobility Inventory (Chambless, Caputo, Jasin, Gracely, & Williams, 1985), which consists of two scales, assessing avoidance when alone and avoid- ance when accompanied by a trusted companion.

General level of anxiety over the previous week was assessed by the Beck Anxiety Inventory (Beck & Steer, 1990), and fear of arousal-related bodily sensations was measured by the Anxiety Sensitivity Index (Peterson & Reiss, 1992). These measures were included because they provide further informa- tion as to the nature of any therapeutic responses in each type of panic disorder.

Degree of respiratory distress over the previous month, arising from full-

120 TAYLOR ET AL.

or limited-symptom panic attacks, was assessed by a 4-item scale developed for the purposes of the study. The patient was asked to rate the extent that he or she was troubled by each of the following thoughts over the past month: "I am going to suffocate" "I have a lot of difficulty with my breathing" "I am short of breath" and "I am going to run out of air to breathe" Ratings were made on a 5-point scale, ranging from 0 (not at all troubled) to 4 (ex- tremely troubled). For the present sample this 4-item scale had good internal consistency (coefficient a --- .89).

Treatment

Patients received ten 1-hour weekly sessions of CBT for panic disorder and agoraphobia, as described in the manuals by Clark and Salkovskis (1987) and Craske and Barlow (1989). The treatment format followed that of Craske and Barlow. Clark and Salkovskis' manual was used primarily as a source of guidance for conducting cognitive restructuring and symptom-induction exercises. We departed from the Craske and Barlow protocol by allocating less time to the treatment of agoraphobic avoidance (i.e., less time devoted to planning and reviewing in vivo exposure to situations such as shopping malls, bridges, tunnels, etc.). Thus, our treatment consisted of 10 sessions rather than the 12 sessions described by Craske and Barlow.

During the early sessions, patients were educated about the nature of panic, anxiety, and avoidance, and presented with the cognitive model of panic attacks (Clark, 1986). In subsequent sessions, patients were trained in coping strate- gies (e.g., respiratory control) and shown how to identify and test catastrophic beliefs about bodily sensations, and encouraged to test these beliefs in weekly homework assignments. Symptom-induction tasks (e.g., voluntary hyper- ventilation, breathing through a narrow straw) also were conducted during therapy sessions as a means of further reducing the patient's tendency to be- come alarmed by harmless bodily sensations. These exercises are described in detail in the treatment manuals (Clark & Salkovskis, 1987; Craske & Barlow, 1989).

Design and Procedure

Potential patients were screened for suitability during a short telephone interview, which consisted of questions from the ADIS-R panic disorder module. Potentially suitable patients were invited to the clinic for an assess- ment consisting of the entire ADIS-R interview and self-report questionnaires. Interviews were conducted by a trained assessor (psychologist, predoctoral intern, or BA-level psychology graduate). Each interview was supervised by a doctoral-level psychologist who assigned diagnoses.

To assess the interrater reliability for the diagnosis of panic disorder, 29 audiotaped ADIS-R interviews were independently reviewed by a second psy- chologist. The interviews were of patients accepted into the study and of those excluded because they did not meet inclusion/exclusion criteria. Interrater reliability for the diagnosis of panic disorder was high (~c = .86). Raters dis-

COGNITIVE BEHAVIORAL THERAPY FOR PANIC DISORDER 121

agreed on only 2 patients, both of whom were not included in the present study. Raters agreed that panic disorder was present in 13 patients and absent in 14 patients.

Treatment was conducted on an individual basis. Therapists were doctoral level psychologists, or predoctoral psychology graduates trained in CBT. Ther- apy sessions were audiotaped and therapists received weekly supervision from the authors. Project staff served as assessors and therapists, although no staff member treated a patient that he or she had assessed. Assessors and therapists were blind to the aims of the study. Assessment measures (ADIS-R and questionnaires) were completed before and after treatment, and at 3-month follow-up.

Results

Group Classification In the absence of an established method for identifying suffocation pan-

ickers and nonsuffocation panickers, we decided to use an empirical method (cluster analysis) for drawing this distinction. Patients were classified as suffo- cation panickers or nonsuffocation panickers on the basis of Ward's (1963) method of cluster analysis, using standardized cluster variables and squared Euclidean distance as the proximity metric. Three cluster variables were used: (1) intensity of dyspnea during the patient's most severe panic, (2) intensity of dyspnea during the patient's most recent panic, and (3) degree of respiratory distress over the past month. The analysis yielded a 2-cluster solution. Table 1 shows the descriptive statistics for each cluster variable. The table shows that on all measures, Cluster 1 patients (labeled suffocation panickers) had significantly higher scores than Cluster 2 patients (labeled nonsuffocation pan- ickers). Thus, the analysis was successful in identifying two clusters of panic- disordered patients, corresponding to those predicted by Klein (1993).

The clusters did not differ in terms of age, gender proportion, marital status, or proportion of Caucasians, ps > .09. Although the clusters differed in their severity of respiratory distress during their most recent and most severe panic attacks (Table 1), the clusters did not differ in the severity of other symptoms of their most recent panic attacks or most severe panics, ps > .05. Table 2 shows the pretreatment means and SDs for the outcome measures. The clusters did not differ on any of these measures, or in the duration of panic disorder or proportion of agoraphobics in each cluster, ps > .1.

Response to Treatment There were no treatment dropouts, and 3-month follow-up data were avail-

able for all but two patients (1 suffocator and 1 nonsuffocator). Table 2 shows the descriptive statistics for posttreatment and 3-month follow-up. Treatment outcome was assessed by computing effect sizes (using Cohen's, 1988, d sta- tistic) to assess changes in symptom severity from pre- to posttreatment, and from pretreatment to follow-up (see the footnote to Table 2 for the formula

122 TAYLOR ET AL.

TABLE 1 COMPARISON OF CLUSTERS ON VARIABLES USED IN CLUSTER ANALYSIS

Cluster 1 Cluster 2 Suffocation Nonsuffocation Panickers Panickers (n = 13) (n = 9)

Pretreatment Variable M SD M SD t (20)

Dyspnea severity during most severe panic 3.2 0.7 1.2 1.2 4.80** Dyspnea severity during most recent panic 2.5 0.9 0.4 0.7 5.89** Respiratory distress-past month 9.2 5.0 5.4 1.3 2.17"

* p < .05, ** p < .0005.

used for computing d values). We also assessed outcome with analyses of co- variance, using pretreatment scores as covariates, cluster membership as the independent variable, and posttreatment and follow-up measures as dependent variables. There were no significant differences between clusters on any of the outcome measures at posttreatment or follow-up, allps > .1. [All Fvalues were < 1 at posttreatment and follow-up, with the exception of two variables: posttreatment avoidance alone (Mobility Inventory), F(1, 17) = 1.67 (data missing for two cases), and posttreatment Beck Anxiety Inventory, F(1, 19) = 1.33.]

Effect sizes (d values) are present in Table 2. These are more informative than p values in interpreting the magnitude of treatment-related response. Cohen's (1988) classification scheme was used to evaluate the magnitude of effect sizes. Here, small effects are ds from 0.20 to 0.49, medium effects are 0.50 to 0.79, and large effects are >I 0.80. Table 2 shows that at posttreatment and follow-up both clusters had large effect sizes for almost all outcome mea- sures. The only exceptions were three medium-sized effects for nonsuffoca- tion panickers. Thus, contrary to the prediction from Klein's (1993) theory, treatment was associated with substantial reductions in symptoms in suffo- cation panickers, and the magnitude of treatment response was equal to (or slightly larger than) that of nonsuffocation panickers. For 5 of 7 measures at posttreatment, and 4 of 7 measures at follow-up, there was a nonsignificant trend for effect sizes of suffocation panickers to be greater than those of non- suffocation panickers.

The mean reduction in panic frequency, from pre- to posttreatment, was 9.5 panics/month for suffocation panickers, and 4.8 panics/month for nonsuffocation panickers. The mean reduction from pretreatment to follow-up was 9.5 panics/month for suffocation panickers, and 5.2 panics/month for nonsuffocation panickers. At the end of treatment, the clusters had similar proportions of patients who were panic-free over the previous month; 46% of suffocation panickers versus 56% of nonsuffocation panickers. At 3-month follow-up 75% of suffocation panickers were panic-free over the previous month

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124 TAYLOR ET AL.

compared to 50% of nonsuffocation panickers. Due to small sample sizes, the trends were not significant (ps > .1). Note that the results for 3-month follow-up are in the opposite direction to those predicted by Klein's theory.

Finally, we sought to determine the proportion of treatment responders and nonresponders in each cluster. Criteria to define "responders" and "nonre- sponders" are arbitrary, and there is no universally accepted definition of these outcome states. Himadi, Boice, and Barlow (1986) proposed that treatment responder status is attained when the patient demonstrates at least a 20% im- provement on at least three of five outcome measures. The measures used by Himadi et al. consisted of measures of panic frequency, global severity, and agoraphobic fear and avoidance. In the present study we did not use mea- sures of global severity. Instead, we defined four logically distinct symptom domains to identify responders, as measured by the following variables: (1) panic frequency (panics/month), (2) fear of panic symptoms (as assessed by the ADIS-R fear of panic scale and the Anxiety Sensitivity Index), (3) agora- phobic avoidance (as assessed by the two scales of the Mobility Inventory and by the ADIS-R measure of agoraphobic avoidance), and (4) anxiety level (as assessed by the Beck Anxiety Inventory). To compute scores for symptom domains defined by composite measures (i.e., domains 2 and 3), the com- ponent measures were converted to T scores (mean = 50, SD = 10) and then the mean of the components was computed. Tscores for a given measure were computed by subtracting the obtained score from the pretreatment mean (for the entire sample), and then dividing by the pretreatment SD.

Patients were classified as responders if they had a 20% or greater improve- ment in at least three of the four symptom domains. Otherwise, patients were defined as nonresponders. Using this criterion, 62% of suffocation panickers and 67% of nonsuffocation panickers were classified as treatment responders at posttreatment, and 75% of suffocation panickers and 63 % of nonsuffocation panickers were classified as treatment responders at follow-up. The propor- tion of responders did not differ between clusters at posttreatment, X2~11 < 1, or follow-up, ~2c1~ < 1.

Discussion

Contrary to the prediction derived from Klein's (1993, 1994) theory, CBT was generally as effective for suffocation panickers as for nonsuffocation pan- ickers, with large reductions in panic frequency, agoraphobia, and related vari- ables. Gains were maintained at 3-month followup. It could be argued that the sample size was not sufficiently large to detect differences in treatment response. Given the small sample size our findings should be regarded as pre- liminary and followed up with studies using larger samples. Even so, there were several trends in the opposite direction to those predicted by Klein.

Our procedure for classifying patients as suffocation panickers or nonsuffo- cation panickers was based on responses from interviews and self-report mea- sures. It may be objected that behavioral or biological tests (e.g., CO2 inha- lation challenges) are required for such a classification. However, Taylor and

COGNITIVE BEHAVIORAL THERAPY FOR PANIC DISORDER 125

Rachman (1994) found that the suffocation fear sca le -a questionnaire mea- sure of suffocation-alarm sensitivity-predicted responses to a behavioral suffo- cation challenge. Participants with high scores on this scale, compared to par- ticipants with low scores, were more likely to panic when they breathed for 2 min through a narrow straw. McNally and Eke (in press) found that this scale also predicted anxiety evoked by COs inhalation challenges. 1 These studies support the use of self-report measures as a way of identifying people with putative hypersensitive suffocation monitors. However, exclusive reliance on self-report measures is a limitation of the present study. In future studies it would be useful to use multiple sources of information to identify suffocation panickers, including self-report measures and behavioral challenges. This may improve the accuracy in determining cluster membership.

Our proportions of panic-free patients were not as high as those obtained by Barlow and colleagues (e.g., Barlow et al., 1989) or by Clark et al. (1994) (i.e., 85-90%), although they were similar to the rate found in other recent studies (25-66%: Black et al., 1993; Shear et al., 1994). Despite these differ- ences, our findings suggest that CBT is effective for suffocation panickers and for nonsuffocation panickers. An important question is which CBT methods are optimal for treating each cluster. Although we did not collect systematic data on the treatment methods, our therapists were most likely to use suffo- cation challenges (e.g., breathing through a narrow straw) in treating patients with prominent suffocation fears. These methods were used to refute catastrophic beliefs (e.g., to challenge the belief that mild dyspnea will lead to suffoca- tion). Klein's (1993) theory suggests that this intervention should trigger suffo- cation false alarms (i.e., increasing panic frequency, at least in the short-term). It may be that repeated exposure to these exercises produces some form of habituation, thus dampening the sensitivity of the alarm monitor (cf. Klein). Thus, CBT may influence the physiological effect of the suffocation alarm mechanism. It remains to be seen whether suffocation panickers can be suc- cessfully treated with CBT methods that do not involve these challenges. It also remains to be determined whether there are types of panic disorder that differentially respond to CBT.

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' This scale was available prior to commencing the present study (Rachman & Taylor, 1993). However, it was not used here because we discovered its value as a measure of suffocation-alarm sensitivity (Taylor & Rachman, 1994) only after the present study was well underway.

126 TAYLOR ET AL.

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RECEIVED: June 16, 1995 ACCEPTED: September 29, 1995