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Cognitive theories of panic disorder suggest that the catastrophic misinterpretation of bodily sensations is the trigger for a panic attack. A challenge to cognitive theories is the suggestion that dyspnea (shortness of breath) is central to the development of panic and that negative cognitions are by-products of panic. To examine these seemingly contradictory theoretical perspectives, the present study investigated panic symptomatology in a sample of patients with chronic shortness of breath (i.e. pulmonary patients). Past studies have shown an increased prevalence of panic in pulmonary patients, a finding that may be useful in elucidating panic etiology. The current sample of pulmonary patients (N=28) confirmed previous reports of high prevalence rates of panic in this population. Based on self-report of panic symptomatology, a total of nine patients (32%) met DSM-IV criteria that were consistent with panic disorder. Multivariate comparison of participants with and without panic symptomatology revealed that panickers had significantly higher levels of anxiety, depression and agoraphobic cognitions. However, these groups showed no significant differences on physiological measures of pulmonary functioning. The authors conclude that dyspnea alone is inadequate in predicting panic development. High levels of panic symptomatology in pulmonary samples may reflect increased opportunities for these patients to misinterpret bodily sensations and, in particular, their pulmonary symptoms.

The cognitive model of panic proposed by Clark (1986)has been extremely influential in the empirical study of panic. According to this model, panic results from the catastrophic misinterpretation of bodily or mental sensations. Specifically, in individuals with panic disorder, sensations commonly associated with anxiety are interpreted as much more dangerous than is actually the case. Not only are these sensations interpreted as dangerous, they are also thought to signal immediate danger (Clark, 1988). For example, an individual may experience breathlessness, heart palpitations, dizziness or other sensations associated with anxiety. These triggers lead to a state of increased apprehension, which in turn leads to an increase of anxiety provoked bodily sensations. These additional sensations are then interpreted in a catastrophic manner. This process builds upon itself with increasingly greater levels of anxiety (Craske & Barlow, 1993). The result is a vicious cycle of sensations, apprehensions and catastrophic thoughts that eventually culminate in a panic attack. Anticipatory anxiety, a fear of additional panic attacks, may predispose a person to future panic attacks. The model of Clark (1986)accounts for panic attacks that occur with anticipatory anxiety by suggesting that the anxiety leads to an increased focus on bodily functioning, thus triggering the panic cycle. A hallmark of panic, however, is that panic attacks frequently occur unexpectedly or `out of the blue'. According to the cognitive theory, attacks that occur without anticipatory anxiety are triggered by bodily sensations from an emotional state other than anxiety. Cox (1996)expanded upon Clark's cognitive model by suggesting an interactional view of panic etiology. He theorized that an individual's susceptibility to the development of panic is determined by the interaction of a trait and congruent trigger. The trait, a cognitive disposition (e.g. state anxiety) representing specific, ideographic vulnerabilities, may involve beliefs associated with bodily symptoms as well as concerns about other areas (e.g. social evaluation). Each individual's cognitive disposition will interact only with certain triggering stimuli. Cox suggests that, although the trigger may be external or internal, it must connect in a `meaningful' way with the trait. For instance, the belief that dyspnea has negative health consequences will be triggered most often by shortness of breath and not by feelings of dizziness or other symptoms often associated with panic. The subjective interpretation of the trigger is clearly important. Ultimately, the individual must accept or reject the association between the trait and trigger. Once an association has been made, the person may then develop catastrophic cognitions and continue on to develop a panic attack. While this cognitive theory of panic is presently very popular, it is not without its critics. Some more persistent challenges to cognitive models come from biomedical models that stress the importance of respiratory distress in the development of panic. 1.1. Dyspnea–fear theory Ley, 1989 and Ley, 1994proposed the dyspnea–fear theory of panic, in which he suggested that hyperventilatory panic attacks arise from an innate emotional response to severe dyspnea or shortness of breath. In this model, fear experienced in the context of breathlessness is given primacy in the development of panic. The fear experienced during panic attacks is derived from the misattribution of the somatic consequences of hyperventilation. The dyspnea–fear theory explains the presence of catastrophic cognitions as a consequence of breathing difficulties on brain function. Over breathing results in hypocapnia, the excessive loss of carbon dioxide (CO2), which causes an increase in blood pH and a decrease in blood and oxygen available to body tissues. Consequently, to maintain proper oxygen levels, an individual must breathe more rapidly and the heart must beat faster. This can result in other symptoms of physiological arousal such as dizziness, lightheadedness and heart palpitations (Edelmann, 1992; Smoller, Pollack, Otto, Rosenbaum & Kradin, 1996). In addition, hypocapnia has detrimental effects on tasks of intellectual functioning, perceptual motor abilities and word association tests (Ley, 1989). Ley (1989)posits that the catastrophic cognitions that accompany panic attacks may be a result of hyperventilation, thus suggesting a physiological explanation for negative cognitions. The presence of dyspnea does not imply the existence of panic, however, because the presence or absence of panic is mediated by level of perceived control (Ley, 1989). For example, a submerged swimmer is not likely to develop fear of dyspnea as long as he/she is submerged as a result of personal volition. Although experiencing similar levels of dyspnea, a swimmer forcibly restrained underwater will likely experience fear due to the lack of personal control (Ley, 1989). Ley believes an analogous process to be at work in hyperventilatory panic attacks, and research has shown dyspnea to be a prominent symptom in hyperventilatory panic attacks (Ley, 1985a and Ley, 1985b; Rachman, Levitt & Lopatka, 1987). In support of the dyspnea–fear theory, researchers point to caveats in cognitive models. For example, some research indicates that the catastrophic misinterpretation of bodily sensations does not occur until after a panic attack has begun, thus suggesting that the catastrophic cognitions are by-products of panic and not responsible for the development of panic ( Ley, 1985a; Wolpe & Rowan, 1988). Further, some panic attacks, including nocturnal panic attacks, may occur without fearful cognitions ( Rachman et al., 1987; Ley, 1989). The majority of persons who experience panic during sleep do so without any connection to dreams or thoughts preceding the attack ( Ley, 1989; see also Margraf, Taylor, Ehlers, Roth & Argas, 1987; Craske & Barlow, 1989). While these issues present challenges to the cognitive theories of panic etiology, they do not provide direct support for biomedical theories such as the dyspnea–fear theory. There is, however, an area of the literature that does link respiratory distress with panic. 1.2. Pulmonary disease and panic Research has consistently shown an increased prevalence rate of panic among persons with chronic obstructive pulmonary disease (COPD). COPD is a broad term used to describe several diseases of the respiratory system, primarily chronic bronchitis and emphysema (National Institutes of Health, 1993). Persons with advanced, chronic asthma also may be considered to have COPD when their condition deteriorates to the point that the airway obstruction is essentially irreversible (Williams, 1993). In a study of COPD patients, clinical interviews indicated that 40% were diagnosed with either depression or anxiety, with panic disorder accounting for the largest percentage (24%) of patients (Yellowlees, Alpers, Bowden, Bryant & Ruffin, 1987). In contrast, lifetime prevalence rates for panic disorder in the general population are estimated to be between 1.5 and 3.5% (APA, 1994). Thus, the prevalence rates reported in COPD patients are greater than those one would expect to find in the general population, a finding supported by several studies (see Table 1). However, as indicated in the table, the prevalence rates of panic disorder in COPD vary widely with estimates ranging from 8 to 67%. Despite this variability, even the most conservative estimates of panic disorder are substantially greater than what would be expected in the general population. Table 1. Prevalence rates of panic disorder in respiratory patients Study Total N Panic disorder Percentage Porzelius et al. (1992) 48 18c 37 Carr et al. (1992)a 93 21d 22.6 Yellowlees et al. (1987) 50 12e 24 Karajgi et al. (1990) 50 4f 8 Pollack et al. (1996)b 9 6f 67 a Respiratory subjects consisted of asthmatic patients only. bA total of nine patients out of 115 were determined to have COPD. cMobility Inventory of Agoraphobia. dSelf-report questionnaires based on ADIS-R and DSM-III-R. ePsychiatric interview based on DSM-III-R. fStuctured Clinical Interview-DSM-III-R (SCID). Table options The association between panic and respiratory disease suggests that respiratory distress may play a role in panic etiology. However, investigations of the relationship between pulmonary disease and panic attacks remain equivocal in supporting the centrality of respiratory distress in the development of panic. The relationship among pulmonary function, dyspnea and panic has been directly assessed with physiological measurements of expiratory gases (Asmundson & Stein, 1994). The technique, known as spirometry, has indicated that panic patients with low levels of pulmonary functioning have more respiratory symptomatology and more negative cognitions than panic patients with higher levels of pulmonary functioning. Although these results show an association between level of respiratory functioning and panic symptomatology, an attempt to replicate and extend this study failed to support the earlier findings (Spinhoven, Onstein & Sterk, 1995). This led the authors of the latter study to conclude that the ``existence of a distinct subgroup of panic patients with signs of actual airway obstruction leading to uncontrollable dyspnea and fear of suffocation remains questionable'' (p. 457). Few studies have examined the developmental antecedents of panic in the context of pulmonary disease. In one study with asthmatics, researchers tested groups of subjects with panic disorder, asthma or no history of anxiety (Carr, Lehrer & Hochron, 1992). Although, it was hypothesized that equating the groups on dyspnea would make them indistinguishable on measures of anxiety, results indicated that ``panic symptoms in asthma, but not panic disorder, are mediated predominately by the experience of dyspnea'' (p. 258). The researchers suggested that processes other than those proposed by the dyspnea–fear theory were at work in panic disorder, a conclusion further supported by research with pulmonary patients (Porzelius, Vest & Nochomovitz, 1992). In this latter study, progression from physical sensations to panic was associated with agoraphobic cognitions but not respiratory measurement or generalized mood state. Further, the patients with panic reported a greater number of negative cognitions and bodily concerns. In sum, it appears that there is an association between respiratory disease and panic. Although research generally indicates that pulmonary disease is not the primary agent responsible for panic development, it does point to the importance of cognitive factors in the development of panic. Surprisingly though, there have been few (if any) attempts to use cognitive models to explain increased levels of panic in pulmonary patients. 1.3. Cognitive model and panic The model of Clark (1986)suggests that the increased numbers of bodily sensations associated with pulmonary disease would present many opportunities for cognitive misinterpretation to occur, thus leading to panic. Yet, it is not the increased number of opportunities alone that lead to panic. There are individuals who experience increased bodily sensations who do not have increased levels of panic (e.g. athletes). Clark has suggested that avoiding or discounting catastrophic beliefs during initial episodes of increased bodily sensations will reduce the likelihood of panic. Clark (1988)states: ``if during a first panic attack a relative or general practitioner gives the patient a clear, noncatastrophic explanation for the bodily sensations that are experienced, a negative interpretative style and further attacks are unlikely to develop'' (p. 77). Although this may explain why some individuals with increased bodily sensations do not develop panic attacks, this does not appear to be applicable to pulmonary patients. It seems that patients with compromised respiratory functioning would have ample noncatastrophic physiological explanations for their bodily symptoms, yet a large percentage go on to develop panic. One possible explanation for the increased prevalence of panic in pulmonary patients is that the bodily sensations experienced as a result of pulmonary disease may reflect actual danger rather than imagined threat. This then suggests an important distinction between individuals with increased bodily sensations who go on to develop panic versus those who do not. Athletes may experience increased sensations, but the sensations likely do not reflect actual danger. The sensations experienced as a result of pulmonary disease may reflect actual danger and thus lead some patients to develop panic. Pulmonary patients with panic would then be seen as similar to other persons who panic but who do not have concomitant pulmonary disease. Both groups may be reacting to misinterpretations of bodily sensations. The difference between them, however, is that one group is reacting to an imagined threat whereas the other is reacting to potential danger. The original model of Clark (1986)emphasizes the misinterpretation of bodily sensations, but does not speak to interpretations that may represent actual danger. Given their compromised physiological functioning, the reactions of pulmonary patients to bodily sensations may not reflect misinterpretations. This paper, therefore, proposes an extension of the cognitive model of panic developed by Clark (1986). Heart palpitations or respiratory distress may reflect actual danger to a pulmonary patient, not imagined threat. Thus, panic reactions could be viewed as a possible response to bodily threat whether the threat is real or imagined. This does not imply that a panic response is the most adaptive way of responding nor the only way of responding. The majority of persons with COPD have similarly compromised physiological functioning without the concomitant panic symptomatology. However, some pulmonary patients may respond to physiological distress in a manner similar to individuals with panic disorder who do not have compromised physiological functioning. Both groups of individuals may react to perceived danger in a way that perpetuates the negative cycle of fear proposed by the cognitive model. The only difference between groups being the presence of real versus imagined threat. The present study sought to further explore the relationship between pulmonary disease and panic symptomatology. A preliminary aim of this study was to examine the relationship between COPD and psychological distress. Consistent with prior studies, it was hypothesized that persons with COPD would report an increased prevalence of panic and generalized anxiety and, that patients with panic would report greater depression (Yellowlees et al., 1987; Karajgi, Rifken, Doddi & Kolli, 1990; Kellner, Samet & Pathak, 1992; Porzelius et al., 1992). The primary goal of this study was to explore the relationship between panic and pulmonary disease and the proposed extension of Clark's cognitive model. From this point of view, chronic pulmonary disability would present a continual array of bodily sensations that could be misinterpreted in a catastrophic manner. A catastrophic misinterpretation, despite the fact that the symptoms could represent actual danger, may lead to the development of panic. Thus, it was hypothesized that COPD patients with panic symptomatology would have significantly more negative cognitions than those without panic symptomatology. On measures of physiological functioning, however, a significant difference between groups was not anticipated. These associations will provide preliminary support for the expansion of the cognitive model of panic suggested in this paper. Alternatively, the dyspnea–fear model, which posits that the experience of physiological distress and a lack of anxiety control will be greater in participants with panic symptoms, will be supported if results indicate a significant relationship between pulmonary functioning and the presence/absence of panic. This would suggest that physiological functioning may in fact contribute to the development of anxiety independently of negative cognitions. Thus, pulmonary functioning would be predictive of panic. Nonsignificant differences between panic and nonpanic groups with regard to negative cognitions would also be expected because the cognitions could be considered a by-product of some, but not all panic attacks.