Panic

Psychological Perspectives

S. Rachman, Jack D. Maser

• Publisher: Routledge
• Year: 2013
• eBook ISBN: 9781134735495
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

The topic of panic has been dominated by biological studies in many areas of anxiety research. This collection of papers, resulting from the National Institute of Mental Health Conferences, presents the viewpoints of clinical researchers assessing the state of the anxiety field. Contributors to this volume argue that biological data can be encompassed in psychological theory.

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Panic:

Psychological Contributions

S. Rachman

University of British Columbia

Jack D. Maser

Affective and Anxiety Disorders Research Branch, NIMH

Introduction

Our aim in compiling this volume is to inform students of psychopathology about recent findings on the subject of panic, and to promote attention to the extremely stimulating psychological perspectives on panic. This collection of chapters by psychologists and psychiatrists should prove to be a convenient medium for readers who wish to become familiar with contemporary thinking on this subject.¹

The importance attached to the concept of panic is largely a result of the research carried out by Dr. Donald Klein and his colleagues over the past 20 years. It is not surprising, therefore, that his conception of the nature of panic as essentially a biological disorder, categorically distinguishable from other forms of mental disorder, was taken as authoritative. The reader is referred to Tuma and Maser (1985) for extensive considerations of this approach. Panic: Psychological Perspectives presents alternatives to a purely biological explanation of panic. The involvement of biological events and processes is accepted, but the contributors’ ideas go beyond this acceptance and their data defy a purely biological explanation.

Definitions

According to the revised third edition of the Diagnostic and Statistical Manual (DSM-III-R; American Psychiatric Association, 1987) the essential features of a panic attack are discrete periods of intense fear or discomfort, and at least four of the following symptoms which appear during each attack: dyspnea (shortness of breath) or smothering sensations; choking; palpitations or accelerated heart rate (tachycardia); chest pain or discomfort; sweating; dizziness, unsteady feelings or, faintness; nausea or abdominal distress; depersonalization or derealiztion; numbness or paresthesias (tingling sensations); flushes (hot flashes) or chills; trembling or shaking; fear of dying; and fear of going crazy, or doing something uncontrolled.

During some of the attacks at least four of these symptoms develop suddenly and increase in intensity within 10 minutes of the first noticed symptom. Episodes involving fewer than four symptoms are called “limited symptom attacks.” As the course of the disorder proceeds particular settings (e.g., in a car, in the market, on an elevator) may become associated with having a panic attack. The individual may fear having a panic attack in this setting, but is uncertain as to its timing or whether or not it will occur at all.

The Manual specifies that an organic etiology is excluded as a cause of these manifestations, and the disturbance must persist for at least 1 month beyond the cessation of any precipitating organic factor. DSM-III-R also states that the attack must be (a) unexpected, that is, not occur immediately before or on exposure to a situation that almost always caused anxiety, and (b) not triggered by situations in which the individual was the focus of others’ attention.

In order to reach a diagnosis of panic disorder there is an additional criterion. Four attacks must occur within a 4-week period, or one or more attacks must be followed by a period of at least a month of persistent fear of having another attack.

There are two subtypes of panic disorder: panic disorder with agoraphobia and agoraphobia without history of panic disorder. Many believe that the etiology of agoraphobia results from the occurrence of panic attacks and that the patients with the former subtype far outnumber patients who have agoraphobia without panic. This issue will be discussed later in our chapter, but figures on the incidence of each subtype must await population-based epidemiology studies.

The DSM-III-R conception of panic disorder is strongly influenced by Klein’s approach, which has been to categorize symptoms into syndromes. Some of the authors in this volume do not agree with the position of a separate category for panics, and they question the justification for viewing panic as other than an intense fear with rapid onset.

Background

Episodes of panic have been known under different names for many years (see Gelder, 1986), and numerous biological explanations have been proposed, including those based on hypoglycemia (see Gorman, Martinez, Liebowitz, Fyer, & Klein, 1984), mitral valve prolapse (Pariser, Pinta, & Jones, 1978), vestibular dysfunction (Jacob, Moller, Turner, & Wall, 1985), and thyroid disease (Hall, 1983; Lindemann, Zitrin, & Klein, 1984). None of these explanations has been confirmed (Fishman, Sheehan, & Carr, 1985; Gorman et al., 1984; Gorman et al., in preparation; Uhde, Vittone, & Post, 1984); psychodynamic theory also has its explanations, but these are essentially untestable.

Studies of the effects of antidepressant drugs on panic (Klein, 1964) first suggested that panic can be dissociated from generalized anxiety and agoraphobia. Then sodium lactate infusion (Pitts & McClure, 1967) was revived as a means of inducing panic (Klein, 1981; Liebowitz et al., 1984), and other compounds were also discovered to be capable of inducing panics (e.g., yohimbine; see Charney, Heninger, & Breier, 1984; caffeine, see Uhde, Roy-Byrne, Vittone, Boulenger, & Post, 1985). These two sets of findings (antidepressant effects and drug-induced panics) formed the foundation for the biological explanation of panic. However, there is no unifying, satisfying explanation of the original or subsequent findings, and the possible role of psychological factors was ignored (Margraf, Ehlers, & Roth, 1986a).

Interest in the psychological aspects of panic emerged rather late. Interviews with persons suffering from panic attacks suggested that cognitive events are related to the onset, timing, course, and consequences of their panics (e.g., Beck, Laude, & Bohnert, 1974). Patients worry and express alarm over the significance of their distressing symptoms; attribute their distress to a variety of causes; think they are going crazy; believe themselves to be in danger of dying or passing out; and often report that during a panic they have a confusing rush of thoughts or “stop” thinking. Convincing evidence of the role of psychological factors in laboratory inductions of panic strengthened the claim that such factors cannot be ignored.

The chapters in this book present information on the cognitions that people report having experienced during a panic, and how these cognitions are related to psychophysiological events. An important contribution of the psychological approach is that it promises to encompass and unify many of the diverse biological findings in a plausible manner.

The Chapters

During the past 3 years, David Barlow and his coworkers have paid particular attention to the relationship between Panic Disorders and other types of anxiety disorders, and this interest is clearly evident in his chapter on phenomenology. Barlow and Craske have organized the material according to a three-system analysis (Lang, 1968; Rachman, 1978). In addition to providing a general review, they consider some important but neglected aspects of panic, notably the occurrence of nocturnal panics, their possible significance for theory, and the importance of the initial panic. They consider the justification for regarding panics as being discontinuous from high levels of fear, and whether or not the term “spontaneous” is an accurate description of certain panic.

In answer to the first question, they cautiously accept the discontinuity hypothesis. Some of the other contributors (e.g., Chambless, Michelson, Turner, and Salkovskis) favor the continuity view, arguing that the evidence points more strongly to a continuum in which panics feature as extreme examples at one end of the continuum. The various contributors to this volume take their turn arguing for and against the proposition that panic is discontinuous from other forms of anxiety.

Turner, Beidel, and Jacob, for example, point out that panic occurs with some regularity in all of the anxiety categories (up to 83% in some of the nonpanic disorders), and that panics also occur in nonclinical samples. Turner et al. challenge the notion that panic disorders are qualitatively distinct, and prefer to construe panics dimensionally, in which panics are placed at the extreme end of a severity scale. The resolution of this issue is more likely to come out of the preponderance of evidence than from a definitive study.

The occurrence of nocturnal panics appears to present a major obstacle to cognitive theories of panic. The argument goes as follows: If panics are induced cognitively, why then do so many patients report that they were awakened by their panic? If these nocturnal panic awakenings occur in the absence of any associated or preceding cognitions, then cognitive theory is incomplete, at least. There are several contrary arguments, however. One is that when a person is awakened at night, for whatever reason, but presumably because of some discomfort, the occurrence or nonoccurrence of a panic depends on how the person interprets his or her perceived discomfort. Another is that dreaming is usually conceived of as a cognitive event, and the individual’s panic might have been triggered by the perceived discomfort induced in the dream. In this context, we might also ask whether there is any relationship between night terrors and nocturnal panic attacks.

Dianne Chambless approaches panic cognitions from the vantage of her excellent work on the cognitive aspects of agoraphobia. As she points out, information about the content and the variations of the cognitions associated with panic is insufficient, but what is known is consistent with the notion that cognitions do play a part in the etiology of panic.

On the basis of her research experience with agoraphobia, she cites pitfalls to be avoided (or at least recognized), and provides suggestions for the collection and interpretation of dependable information on panic cognitions. Dr. Chambless postulates that patients with panic disorder believe that harm is more likely to befall them than other people, and they think more frequently about the possibility of harm, especially somatic harm. They are highly tuned to cues that might signal harm. The question of whether or not these differences are “due to current mood or to enduring characteristics” remains to be dealt with.

Rachman observes in his chapter that while most panics are distressing, the consequences of panic can be disabling. He focuses attention on three types of consequences: behavioral, psychophysiological, and cognitive. Along with Marshall (this volume) and others, Rachman believes that extensive avoidance behavior often is a consequence of panic, but avoidance may also have other origins. Many patients report the development of avoidance in the absence of panics, and as Barlow and Craske point out, panics are reported by patients with psychological problems that do not fit into the diagnosis of panic disorder or of agoraphobia. Patients who are seen in hospital clinics are more likely to report a sequence of panic followed by avoidance.

Presumably, those patients who experience panic which is not followed by disabling avoidance are less likely to seek help at a hospital clinic. For this reason they are likely to be underrepresented in hospital-based prevalence studies. Drawing conclusions solely from clinic samples can be misleading. In order to answer the question of what symptoms follow from other symptoms in the course of an illness, while avoiding Berkson’s Paradox (1946), data from population samples are required.

Data from the population-based NIMH-Epidemiologic Catchment Area studies, particularly those reported by Boyd et al. (1984), are relevant. Table 4 in that report indicates that a person with agoraphobia is 18 times more likely to have panic disorder than someone without agoraphobia. For purposes of comparison, approximately the same odds ratio² (18.8) hold for having panic disorder if one is diagnosed as having an episode of major depression.

Although the odds are high (Boyd, personal communication), one needs to know the number of people occupying the cell defined by persons with agoraphobia and not panic. (This would be cell C in Footnote 2.) In 1986, Weissman, Leaf, Blazer, Boyd, and Florio reported that the lifetime rate of agoraphobia without panic disorder or panic symptoms ranged from 1.4 to 6.6 per 100 in the population. The lifetime rate of agoraphobia with panic disorder symptoms ranged from 1.7 to 2.6 per 100. On the basis of population studies there are many people for whom panic does not precede agoraphobia. Apparently, people with more than one disorder (agoraphobia plus panic) tend to seek help in clinics located in research centers, while those with only one disorder (agoraphobia) are less likely to come to such clinics. Data collected at research clinics, by virtue of an overrepresentation of patients with two diagnoses can give rise to a spurious correlation, even when the two diagnoses have independent probabilities of occurrence (Berkson, 1946).

Using a nonchemical method for inducing panic under controlled environmental conditions, Rachman found that panics tended to be followed by increases in expected fear, but not in reported fear. Unexpected panics contributed most to these changes in prediction, and expected panics had little effect on prediction or on reports of fear. Disconfirmed expectations of panic were followed by reductions in self-reported fear. Panics were followed by increases in the predictions of future panics. Although subjects correctly predicted roughly one in three of the induced panics, they showed a high rate of overprediction.

The possibility that some panics are caused by hyperventilation has been considered from time to time. Salkovskis concludes from his research that while hyperventilation often plays an important role, it is not a necessary condition for the development of a panic. His analysis of the influence of hyperventilation leads naturally to a consideration of other physiological information about panic, and he finds that the data are most consistent with the cognitive model. While acknowledging the strong association between panics and global avoidance behavior, Salkovskis notes that the behavioral components have been construed too narrowly. He also draws attention to the useful point that, contrary to what has been believed for some time, patients with generalized anxiety also show extensive avoidance behavior.

Van den Hout discusses the psychophysiological approach to panic, and attempts an ambitious integration of the psychological and physiological data on the experimental induction of panic. The data are often confusing and sometimes in apparent conflict, but his reconciliation is plausible and the explanation for the conflicting findings is promising and testable. Van den Hout also introduces an interoceptive model of fear that bears a resemblance to Seligman’s outline of a conditioning theory of panic. Despite many attractive features, the concept of interoceptive conditioning does not easily lend itself to investigations of the genesis of panic, and it will need to be defined operationally before progress can be expected. The CR is easily defined, but the identity of the CS, UCS, and UCR is much less clear.

Much of the contemporary work on applying cognitive concepts to anxiety can be traced to the pioneering work carried out in 1976 by Beck. The implications of his work for anxiety were neglected because of the great interest that was then shown in forging cognitive theories of depression. It is only within the last 3 years that his attention, and that of others, has turned to the cognitions that precede, accompany, and follow episodes of panic (Beck & Emery, 1985).

Clark’s theory that panics are induced by catastrophic misinterpretations of bodily sensations is the fullest and most advanced of the products of Beck’s original claim that ideas and images play a vital role in determining anxiety states. It is not surprising to find connections between his writings and those of Beck. Both agree in general terms about the critical importance of ideation, but they differ in detail.

Beck recently added a new proposition to his original work: during panics the person experiences a significant loss of reasoning ability. Confirmation of this claim, or at least a more specifically formulated version of it, would bring to the fore the problem of how to prepare people for experiences in which their cognitive range is suddenly constricted. If it is correct that panics are caused by misinterpretations of bodily sensations, presumably we should try to establish the correct interpretation prior to panic episodes, during which time the person’s ability to reason is reduced. It remains to be seen whether or not this tactic will be complicated by state-dependent problems of transfer of learning.

Clark’s theory of catastrophic misinterpretations is concisely and clearly described. The theory is developed with considerable skill and is then used to incorporate a surprisingly wide range of information. The theory is consistent with the content of the cognitions reported by panic patients, with the sequence of events, the effects of panics induced in the laboratory,...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright
• Contents
• Contributors
• Preface
• 1. Panic: Psychological Contributions
• 2. The Phenomenology of Panic
• 3. Assessment of Panic
• 4. Cognitive and Biological Models of Panic: Toward an Integration
• 5. A Cognitive Model of Panic Attacks
• 6. Cognitive Approaches to Panic Disorder: Theory and Therapy
• 7. Phenomenology, Assessment, and the Cognitive Model of Panic
• 8. Cognitive, Behavioral, and Psychophysiological Treatments and Correlates of Panic
• 9. Combined Pharmacological and Psychological Treatments for Panic Sufferers
• 10. Cognitive Models and Treatments for Panic: A Critical Evaluation
• 11. Cognitive Mechanisms in Panic Disorder
• 12. Fear, Anxiety, and Panic: Context, Cognition, and Visceral Arousal
• 13. The Explanation of Experimental Panic
• 14. Panics and Their Consequences: A Review and Prospect
• 15. An Appraisal of Expectancies, Safety Signals and the Treatment of Panic Disorder Patients
• 16. Competing Theories of Panic
• References and Author Index
• Subject Index