Behav. Res. Thu. Vol. 30, No. 4, pp. 347-351, Printed in Great Britain. All tights reserved
1992 Copyright
0
THE MANY FACES OF PAN: PSYCHOLOGICAL PHYSIOLOGICAL DIFFERENCES AMONG THREE OF PANIC ATTACKS RONALD
State University
of New York
at Albany,
0005-7967/92 $5.00 + 0.00 1992 Pergamon Press Ltd
AND TYPES
LEY
1400 Washington
Avenue,
Albany,
NY 12222, U.S.A.
(Received 26 March 1991; received for publication IO October 1991) Summary-The thesis of this paper is that failure to recognize the psychological and physiological differences among panic attacks within DSM-IIIR precludes meaningful comparisons and evaluations of research findings, confounds theoretical issues, and impairs the development of more specific, and thereby more effective, programs of treatment. To remedy this, a recommendation is made to define panic attacks on the basis of psychological and physiological distinctions that fit three categories of severity: Type I (classic panic attack), Type II (anticipatory panic attack), and Type III (cognitive panic attack). The logical-empirical rationale for the categories recommended is presented in the context of relevant research findings. Implications for theory, experimental design, and treatment are discussed.
The word ‘panic’ has its origins in frightening tricks played on unwary travelers by the Greek God Pan, a clever and mischievous fellow who frequently used disguises to mask his true identity. Panic disorder as defined by the DSM-IIIR (American Psychiatric Association, 1987) classification covers a rather broad range of symptoms, so broad that the classification may have outlived its usefulness, and may, in fact, be the source of tricks that can confound investigations of the disorder. A few recent studies illustrate problems involved in the identification of the necessary components that define a panic attack. Catastrophic cog&ions. Rachman, Levitt and Lopatka (1987) found that fearful cognitions did not occur in 27% (8 out of 30) of the panic attacks experienced by their sample of panic-disorder patients; and Wolpe and Rowan (1988) found that when they do occur, they follow, rather than precede, the fearful event of the attack. None the less, a cognitive theory of panic attacks (viz. Beck, 1987) rests squarely on the assumption that catastrophic cognitions, which are assumed to be a consequence of the misinterpretation of symptoms, account for the fear experienced in panic attacks. Thus, while catastrophic cognititions rank high among the symptoms of the DSM-IIIR classification of panic attacks, they are not a necessary component of panic. Tuchycardiu. Palpitations and other symptoms of coronary artery disease are frequently reported to occur during panic attacks. However, findings from studies which attempt to induce panic attacks in panic-disorder patients by means of prolonged inhalation of 5% COz in air are not consistent. While Woods, Charney, Goodman and Heninger (1988) report a significant increase in heart rate for patients who experience attacks during inhalation of 5% CO,, Sanderson, Rapee and Barlow (1989) and Craske and Barlow (1990) do not. Paradoxically, in a single-case study in which the S was selected from among those of the Sanderson et al. (1989) sample, Sanderson, Rapee and Barlow (1988) reported a sharp increase in heart rate from 86 to 105 bpm, a finding which is consistent with earlier reports of tachycardia in adventitious panic attacks (i.e. Cohen, Barlow & Blanchard, 1985; Margraf, Ehlers & Roth, 1987; Lader & Mathews, 1970). Since tachycardia is not common to all panic attacks induced by the 5% CO, challenge, this frequently reported symptom of the DSM-IIIR classification appears not to be a necessary component of panic. Hyperventilation. Although Ley (1985b, 1989) has placed heavy emphasis on the central role of the sequelae of hyperventilation in the producton of dyspneic-fear and the common symptoms of panic attacks, Hibbert and Pilsbury (1988) reported a test trial of transcutaneous monitoring of pC0, in which one of four patients who claimed to have a panic attack did not show a concurrent decrease in pC0,. Although almost all the symptoms of panic listed in the DSM-IIIR classification are common effects that can be produced by hyperventilation, it appears that hyperventilation may not be a necessary component of panic. Furthermore, since prolonged inhalation of 5% CO, 347
RONALD LEY
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precludes the possibility of hypocapnea, panic attacks reported during such inhalations cannot be the result of hyperventilation. DSM-IIIR
and the dejinition of panic
Although the DSM-IIIR classification reflects research findings which make it clear that the sudden onset of intense fear, dyspnea, tachycardia, and catastrophic cognitions are among the most common symptoms of panic attacks, the classification does not specify which symptoms, if any, are essential components that define the panic attack. If there are no essential components and if we accept Beitman, Basha, Flaker, DeRosear, Mukerji and Lamberti’s (1987) contention that there are panic attacks without fear, then a patient who presents, for example, ‘trembling’, ‘hot flushes’, ‘sweating’, and ‘feelings of unreality’ (four symptoms of DSM-IIIR) in association with episodes of intense ‘discomfort’, could be diagnosed as suffering panic disorder (given the necessary frequency and recency of such episodes), though there is no fear, no dyspnea, no tachycardia, and no catastrophic cognitions. While some critics of DSM-IIIR might argue that such a diagnosis would be absurd because it strips ‘panic’ of its basic meaning, the diagnosis in question might be defined by others as a logically valid conclusion. Is it possible to resolve the conflict between the charge of absurdity and the retention of the primary features of the DSM-IIIR, and at the same time find accommodation for the validity of the research findings cited above? The present paper addresses this multi-faceted question and offers an answer in terms of a refined classification of panic attacks. A Panic Attack is not a Panic Attack is not a Panic Attack The identification of the necessary components of panic is, in a sense, part of the theoretical problem, a situation which is bound to breed chaos because conflicting theoretical interpretations cannot be compared and evaluated if they are addressed to different, albeit similar, phenomena. The purpose of the present paper is to describe three distinctly different types of panic attacks, all of which meet the criteria required by the DSM-IIIR classification. The importance of making the distinctions recommended here lies in the clarification of theoretical issues, the facilitation of communication in research, and the development of effective programs of treatment through greater specificity of the underlying complaint. While the categories offered may not exhaust all of the possible types of panic attacks that might fall beneath the DSM-IIIR heading, they are intended to cover the major varieties of attacks discussed in the contemporary professional journals that publish articles dealing with theory and treatment of panic disorder. The idea that there may be more than one type of panic attack is not new: Ley (1987) and Wolpe and Rowan (1988) proposed that panic attacks can be described in terms of a Pavlovian Table I. Psychological/subjective
and physiological/objective
Psychologicol/subjeclive
dis~inclions
(probabiliry
and expected
inlensify)
Fear
terror (extreme dyspneic-fear) with desire to flee
(2)
Dyspnea (difficulty breathing, air hungry, choking, smothering) Palpitations Catastrophic Cognitions
p-high (sense suffocation)
Remaining IIIR
p-high
(5)
Physiological/objecfioe (6)
(7) (8) (9)
symptoms
among three types of panic attacks Type III (Cognitive PA)
(1)
(3) (4)
distinctions
Type II (Anticiuatorv PA)
Type I (Classic PA)
p-high vhigh thoughts)
of DSM-
distinctions
(+
=present,
in drop Sharp PC01 > IO mmHg Sharp increase in respiration rate and/or tidal volume Sharp increase in heart rate > 10 bpm Sharp increase in clectrodermal response
-
of
(‘unreal’
impending
or
bizarre
fear or anticipatory anxiety (strong dread of what may folIOW) p-medium
apprehensive
p-medium *medium (fearful thoughts but not in context of ‘unreality’)
@OW @ow (mundane ful thoughts)
pmedium
p-IOW
= not presenl)
anxiety
p-&W
+
-
+
-
+
_
+
-
4.
-
_
fear-
Three types of panic attacks
349
conditioning paradigm in which a primary hyperventilatory panic attack constitutes the unconditioned response, and a secondary anticipatory attack constitutes the conditioned response. While the present proposal is an outgrowth of this point of view, the categories presented here do not require the assumption of a Pavlovian conditio~ng paradigm. Types of Panic Attacks The classification of panic attacks in terms of three types is based on two sets of criteria: psychological/subjective distinctions and physiological/objective distinctions. Table 1 lists five psychological criteria and five physiological criteria upon which distinctions among the three types of panic attacks are made. Case reports that exemplify each type are given below. Classic panic attack The psychological/subjective distinctions that mark the Type I or classic panic attack were derived from analyses of studies that measured the frequency and intensity of symptoms reported to occur during panic attacks (e.g. Barlow, Vermilyea, Blanchard, Vermilyea, DiNardo Br Cerny, 1985; Ley, 1985a,b; Rachman, Levitt & Lopatka, 1987) and from collateral studies of dyspneic complaints in breathing disorders (e.g. Comroe, 1974; Fenn & Rahn, 1964; Porter, 1970; Timmons & Ley, 1992; von Euler & Katz-Salamon, 1988). The significance and centrality of seemingly uncontrollable dyspnea in conjunction with fear in Type I panic attacks is clear (Ley, 1989; Rachman er al., 1987). As Aiken, Zeally and Rosenthal (1970) have pointed out: Dyspnea may be felt as endangering to life to a greater extent than almost any other symptom: to the patient, the experience of dyspnea is regarded as something which, if it worsens, to asphyxia must inevitably be fatal (p. 256). The Type I panic attack is marked by uncontrolled, high-intensity dyspnea (sense of impending suffocation) and heart palpitations accompanied by terror (extreme dyspneic-fear) together with a strong desire to flee. The catastrophic cognitions that often follow are marked by thoughts associated with death or impending doom. Compared with the Type II and Type III panic attacks, the probability and intensity of experiencing the remaining symptoms of the DSM-IIIR classification are highest. The physiological/objective distinctions that mark the Type I panic attack were derived primarily from analyses of adventitious panic attacks that occurred in a laboratory setting during physiological assessments (Cohen et al., 1985; Lader & Mathews, 1970) or during the administration of treatments in experimental research (Margraf et al., 1987; Sanderson, 1987). The most complete physiological description of a Type I panic attack can be found in a single-case study by Sanderson et al. (1988) based on data all of which came from a single S selected from an earlier experiment by Sanderson (1987). In this earlier experiment, Sanderson required a panic-disorder patient to breathe room air via an inhalation mask during a 5 min baseline period prior to a scheduled 20 min period during which the patient was told that she would be breathing a gas which might produce a panic attack. After 6 min of inhalation of room air (the gas the patient believed could produce a panic attack, i.e. the ‘panic-induction gas’) a panic attack was reported: anxiety increased sharply (Fig. I), heart rate increased from 86 to 105 bpm (Fig. 2), electrodermal response showed a sharp increase in conductivity (Fig. 3), respiration rate increased (Fig. 4), and end-tidal pCO,, which was constant throughout the entire procedure (mean pCOz = 24.5 mmHg, SD = 0.67), fell precipitously from 26 mmHg during the next-to-final minute to 17 mmHg during the final minute when the patient reported a panic attack (Fig. 5). Except for low finger temperature, an effect that was observed during an adventitious panic attack reported by Cohen et al. (1985), all of the physiological markers of a Type I panic attack listed in Table 1 were presented by the patient. Case of a Type I panic attack The following abstract from illustrates the extreme severity cognitive impai~ent, as well experienced. The patient was a
an interview with a panic-disorder patient was selected because it of a Type I panic attack in terms of behavior and evidence of as an intros~tive report of fear and the dominant symptoms 3S-yr-old woman who experienced a panic attack while driving to
3.50
RONALD LEY
8
“Panic-Induction” Air
6
I
Pre
7.5
Minutes
10.0
11.0
&Port Panic
Fig. I. Subjective anxiety ratings during baseline air and panic-induction air. Adapted from Sanderson et n!., 1988.
her home in a suburb of Albany, N.Y. during the first cold and snowy night of winter. She reported that her heart suddenly began to beat wildly as she struggled to breathe. Although she was driving on a dark country highway with no help in sight, she stopped her car in the middle of the road, got out, and started running down the highway. She did not know where she was going or what was happening to her, but that she felt that she was going to die and that she had to leave the car and run away. Her recall of events that followed was vague, but she remembered that it was a truck driver who found her and took her to the emergency room of a local hospital. Anticipatory panic attack
The psychological/subjective distinctions that mark the Type II or anticipatory panic attack were also derived from analyses of studies that measured the frequency and intensity of symptoms reported to occur during panic attacks, especially studies that used prolonged inhalation of 5% CO, as an aversive challenge for provocation of panic attacks (e.g. Craske & Barlow, 1990; Roth, Margraf, Ehlers, Taylor, Maddock, Davies & Agras, 1990; Sanderson et al., 1989; Woods et al., 1988). The C~*-challenge studies provide a unique opportunity to study the occurrence of Type II panic attacks because in addition to meeting the criteria listed in Table 1, inhalation of 5% CO2 in room air precludes the possibility of hyperventilation and its hypocapneic psychological and physiological sequelae. An examination of the fear or anxiety ratings of those Ss who are reported to experience panic attacks during prolonged inhalation of 5% CO2 makes it clear that the intensity of fear reported is significantly less than that experienced during panic attacks in the everyday world (see Craske & Barlow, 1990; Woods et al., 1988) and that the focus of fearful concern is centered on what might happen (i.e. anticipations rather than what is happening. Furthe~ore, the qualitative analysis of panic attacks during inhalation of 5% CO2 makes it equally clear that the terror and desire to flee
351
Three types of panic attacks “Panic-Induction” Air
A
85
80
I
I
I
I
I
I
6
7
8
9
10
11
Minutes
P&c
Fig. 2. Mean heart rate for five I-min periods during baseline air (l-5) and six I-min periods during panic-induction air (6-I 1). Adapted from Sanderson et al., 1988.
that characterize the Type I panic attack are not reported during panic attacks induced by 5% CO*: Roth et al. (1990) reported that of 24 patients who experienced panic attacks during inhalation of 5% CO*, 10 (42%) did not request that the administration of the gas be discontinued While it is highly likely that the occurrence of a panic attack in the relative safety of the laboratory attenuates the intensity of the fear experienced (Ley, 1988b), a comparison of the subjective reports of patients who experienced attacks induced by lactate infusion (e.g. Bonn, Harrison & Rees, 1971; Pitts 8z McClure, 1967) with those of patients whose attacks were induced during inhalation of 5% CO, suggests that factors other than the safety of the laboratory account for the relative diminution in intensity of attacks during inhalation of 5% CO,. As for the symptoms of the DSM-IIIR classification of panic, studies that use the 5% CO, challenge, report lower frequencies and/or lower intensities and/or lower similarity ratings compared with those experienced during panic attacks in the everyday world. Sanderson (1987), for example, compared both the frequency and intensity of 16 symptoms of DSM-IIIR reported by patients during panic attacks induced by 5.5% CO, with the frequency and intensity of symptoms during panic attacks in the natural environment and found the following: Frequency of symptoms. Excluding the sensation of ‘panic or fear’, which was reported by all Ss, Sanderson (1987) found that only three of 15 symptoms (binomial P -c 0.01) were identified to have occurred more frequently during the CO, induced panic attacks: ‘pounding or racing heart’, ‘breathlessness or smothering sensations’, and ‘choking’. It should be noted, in connection with these symptoms, that while prolonged inhalation of 5.5% CO2 will increase ventilation dramatically (minute volume will be increased about threefold) and give rise to dyspnea (especially if Ss attempt to retard breathing by slowing down respiration rate), Sanderson found virtually no increase in heart rate from baseline (M = 82 bpm) to, and throughout, a 15-min period of prolonged inhalation of 5.5% CO, (M = 83 bpm).
352
RONALD LEY
-3.5
“Panic-Induction” Air
Air
-3.0 F
-1.0
s
-0.5
d 8
BL .5
I
I
I
I
6
7
8
9
I
I
10 11 Report Panic
Fig. 3. GSR (J&) changes for five I-min periods during baseline air (i-5) and six I-min periods during panic-induction air (a-1 1). Adapted from Sanderson ef al., 1988.
Intensify of symptoms. Sanderson’s (1987) intensity ratings of symptoms on a scale of l-8 (1 = slightly felt, 8 = very strongly felt) showed an even more remarkable pattern. Except for ‘nausea or abdominal distress’ (5.7 during CO* panic, 5.3 during natural panic), all of the intensity ratings were less during panic attacks induced by 5.5% COz than those during panic attacks in the natural environment, including ‘panic or fear’ (5.4 during COz panic, 7.5 during natural panic). ~fmilarify ratings. While Sanderson’s findings pertaining to differences in the frequency and intensity of symptoms point indirectly to the relatively low similarity between naturally occurring panic attacks and those induced by 5.5% CO*, Craske and Barlow (1990) provide direct evidence of the low similarity. On a nine-point scale (0 = not at all similar, 8 = identical) of similarity of ‘symptoms and feelings to naturally occurring fear/panic reactions’, one group of panic disorder patients (n = 16) gave a mean rating of 3.0 to the similarity of their experiences during a 15 min period of prolonged inhalation of 5.5% CO,, while the other group (n = 18) gave a rating of 3.9. The physiological/objective distinctions that mark the Type II panic attack are limited to occasional sharp increases in heart rate and electrodermal conductivity. Regarding heart rate changes, for example, a more detailed examination of the results of Woods et al. (1988) reveals that the mean heart rate change for all of the 14 patients who breathed 5% CO, increased significantly from baseline by 16 bpm, and for the eight patients who panicked, heart rate increased by 25 bpm. Sanderson (1987), on the other hand, reported no increase in heart rate for patients who panicked and patients who did not. The findings of Craske and Barlow (1990) are also inconsistent with those of Woods et al., but in agreement with those of Sanderson (1987). That is, for a group of 16 panic-disorder patients, Craske and Barlow reported that heart rate at baseline (77.4 bpm, SD = 11.7) was identical with heart rate during inhalation of 5.5% CO2 (77.4, SD = 11.8). Furthermore, for a second group of 18 patients, heart rate at baseline (75.8 bpm) deviated ever so slightly from heart rate during inhalation of 5.5% CO2 (76.0 bpm). Some place
Three types of panic attacks
353
17
16
13
12 Air
“Panic-Induction”
Air
Fig. 4. Mean respiration rate (bpm) for five I-min periods during baseline air (1-5) and six 1-min periods during panic-induction air (6-11). Adapted from Sanderson Ed al., 1988.
in between the extremes of the findings of Woods et al. (1988) and those of Sanderson (1987) and Craske and Barlow (1990), Roth et al. (1990) reported essentially the same small increase in heart rate of approx. 5 bpm for all patients (panickers and nonpanickers alike) and normals from baseline to the period of inhalation of 5% C02. While other physiological indices might show changes in the same direction as those that occur during Type I panic attacks, such changes would not be expected to show consistently the same sharp changes of equal magnitude to those that occur during Type I attacks. A comparison of the findings of Roth et al. with the case studies that illustrate the Type I attack (i.e. Lader & Mathews, 1970; Sanderson et al., 1988) makes this clear. A caveat to be noted in connection with prolonged inhalation of 5% CO, is that such inhalations can lead to a Type I panic attack if the increased ventilation stimulated by the CO2 continues after the termination of the CO*. That is, while the hyperpnea induced by 5% CO, is protected against the production of respiratory alkalosis, prolonged hyperpnea following 5% CO, is not. Therefore, a patient subjected to prolonged inhalation of 5% CO2 is vulnerable to a Type I panic attack in the period immediately following termination of CO,, especially if the assessment procedure immobilizes the S therby restricting the metabolic production of CO, (see Ley, 1988a). Although research findings from analogue studies of the effects of prolonged inhalation of 5% CO, provide data relevant to Type II panic attacks, there is no environment outside the laboratory where air contains 5% CO,. What then accounts for Type II panic attacks in the everyday world? As indicated earlier, the occurrence of Type II attacks can be explained on the basis of Pavlovian conditioning (Ley, 1987; Wolpe & Rowan, 1988). From this point of view, the conditioned stimulus (CS) consists of signals which predict the probable onset of an unconditioned stimulus (UCS) that consists of hyperventilatory hypocapnea or any event that gives rise to severe uncontrollable dyspnea with concomitant dyspneic-fear (UCR-unconditioned response); the conditioned
RONALD LEY
354
“Panic-Induction” Ah
Air 26
25
h 24-
23 -
19 18 -
“12
3
4
5
6
Minutes
7
8
9
10 11 Report Panic
Fig. 5. Mean end-tidal pC0, in mmHg for five I-mm periods during baseline air (l-5) and six I-min periods during panic-induction air (611). Adapted from “The influence of perceived control on panic attacks induced via inhalations of 5% CO, enriched air”, by W. C. Sanderson, 1987, unpublished doctoral dissertation, State University of New York at Albany.
response (CR) consists of fear without dyspnea (anticipatory anxiety) that occurs in response to the CS. While Type II panic attacks might be explained from other points of view, two distinctive implications of a Pavlovian conditioning interpretation should be noted. One is that Type II panic attacks must be preceded by a history of at least one Type I attack. The other is that a Type II panic attack could progress into a Type I attack if the anticipatory anxiety is sufficiently prolonged and/or sufficiently intense to produce the degree of hypocapnea necessary for the induction of severe uncontrollable dyspnea. Case of a Type II panic attack The following abstract illustrates the moderate severity and type of symptoms often reported by a panic-disorder patient during panic attacks induced by prolonged inhalation of 5% CO2 in air. The patient was a young adult woman with a 2 yr history of panic attacks. She reported an attack during inhalation of 5% CO1 in air: (a) mild dyspnea, (b) mild palpitations, (c) weakness, (d) fear of losing control, (e) dread of what might follow. The patient was told before administration of 5% CO* that the gas would increase her ventilation and might produce a panic attack. Cognitive panic attack
The psychological/subjective distinctions that mark the Type III or cognitive panic attack include a relatively mild state of apprehension associated with timidity and lack of assertiveness, in which the terror and strong desire to flee that marks the Type I attack and the anticipatory anxiety (strong dread of what may follow) that mark the Type II attack are missing. The underlying anxiety of the Type III panic attack is probably generated by worry and excessive concern with real, but relatively minor, negative events or major negative events for which the probabilities are low, e.g.
Three types of panic attacks
355
“What will happen to me if my car breaks down when I am alone? What will my parents think of me if I get low grades in school? How would my family get on without me if I died in an airplane crash?” Unlike the Type I panic attack in which the symptoms precede the onset of terror, the Type III attack is marked by occasions in which a relatively low level of chronic anxiety waxes and leads to an increase in arousal which produces symptoms of anxiety which are sufficiently strong to alarm the sufferer, who often makes a catastrophic interpretation of what the symptoms signal. In the case of Type III panic attacks, the anxiety precedes the symptoms. Such increases in anxiety that trigger Type III panic attacks are probably the consequences of a relatively stressful event which cannot be conveniently avoided; e.g. being called on to recite in class, having a flat tyre or accident while driving alone, receiving an anonymous harassing phone call. While a relatively large number of symptoms of DSM-IIIR may be identified by the patient, a careful analysis will typically reveal that the intensity of such symptoms is low compared with those reported to occur during Type I and Type II attacks. The physiological/objective distinctions that mark the Type III panic attack are the absence of any significant changes in functions indicated by the five criteria of Table 1, or, at best, slight manifestations of the symptoms when provoked by thoughts that center on the patient’s primary sources of anxiety. Type III panic attacks reported during physiological assessments will show small or no correlated changes in physiological functions such as breathing and heart rate. Patients identified as sufferers of Type III panic attacks will not be discernible from asymptomatic Ss on standard psychophysiological assessment measures (Bruce Cuthbert and Peter Lang, pers. commun., 18 October 1990), and panic attacks reported during ambulatory monitoring will show little or no correlated change in the physiological variables monitored (e.g. Buikhuisen & Garssen, 1990). Case of Type III panic attack
The follo~ng abstract from an interview with a panic-disorder patient was selected because it illustrates the relatively mild severity of a Type III panic attack in the everyday world. The patient was a passive young adult woman with a 6 yr history of panic attacks that began in a college classroom in a course with an instructor who frightened her because he had a reputation as a ‘hard marker’; the patient was afraid that she might get a low grade and lose her father’s approval. She claimed to have a panic attack during every class period, but remained in her seat and did not leave the classroom until the class was over. She did not miss a single class for the entire semester for fear that it might jeopardize her grade. Her panic attacks were marked by anxiety and most of the other symptoms listed in DSM-III classification, except that she reported that most of the symptoms followed, rather than preceded, the onset of her attacks. DISCUSSION
Theory and research
The implications of the proposed refinement in the definition of panic attack for theory and research are clear. The resolution of some theoretical conflicts among current explanations of panic (e.g. Barlow’s interoceptive conditioning fear-of-fear hypothesis, 1987; Beck’s cognitive-misinterpretation-of-symptoms model, 1987; Ley’s hyperventilation theory, 1985b, 1989) may be found if the results of studies in the future are analyzed in terms of the three types of panic attacks proposed here. That is, conflicting research findings and conflicting theoretical positions based on such findings may be the consequence of critical differences among Ss all of whom are identified as patients suffering panic attacks as defined by DSM-IIIR. Even if the approach proposed here does not resolve conflicting theoretical issues, nothing would be lost, and perhaps greater experimental precision would be gained through increasing the homogenity of experimental groups and thus reducing Beta errors, the bane of the research scientist. That is, the present proposal offers a possible means for improving research designs for the study of panic disorder by providing a basis for increasing statistical precision (i.e. reducing within-group variance) through blocking on the three types of panic and by providing the basis for the determination of interactions among the three types of panic and other experimental treatments or characteristics of the Ss.
356
RONALD LEY
Treatment Unlike some psychotherapeutic approaches in which all complaints receive the same treatment, behavior therapy is based on the assumption that the remedy must be designed to fit the complaint. In the case of panic disorder, differences in treatment and differences in the relative success of treatment may depend to some extent on differences among patients with respect to the three types of panic attacks outlined here. Clearly, breathing retraining would be expected to be most beneficial to patients who suffer Type I attacks, while cognitive approaches would be expected to have the most benefit for those who suffer Type III attacks. Issues of the most efficacious approach aside, keener distinctions among the underlying complaints of patients will lead to improved techniques of treatment and thus deliver the greatest benefits to patients. Although the Greek God Pan often wore disguises that aided him in his cruel and mischievous behavior, he was a safeguard for those who believed in him, for those who saw him for what he was-a complex and many-sided figure.
REFERENCES Aitken, R., Zealley, A. & Rosenthal, S. (1970). Some psychological and physiological considerations of breathlessness. In Porter, R. (Ed.), Breathing: Hering-Breuer centenary symposium. London: Churchill. American Psychiatric Association (1987). Diagnostic and statistical manual of mental disorders (3rd edn). Washington, D.C. Barlow. D.. Vermilvea. J., Blanchard, E., Vermilyea, B., DiNardo, P. & Cerny, J. (1985). The phenomenon of panic. Journal of Abnormal Psychology, 94, 320-328. Beck. A. (1987). Coenitive aDDrOaCheS to nanic disorder. In Rachman, S. & Maser, J. (Eds), Panic: Psychological p&spe&es.‘Hillsdale, N.Jr:-Erlbaum. _ Beitman, B. D., Basha, I., Flaker, G., DeRosear, L., Mukerji, V. & Lamberti, J. (1987). Non-fearful panic disorder: Panic attacks without fear. Behaviour Research and Therapy, 25, 487492. Bonn, J., Harrison, J. & Rees, W. (1971). Lactate induced anxiety: Therapeutic applications. British Journal of Psychiatry, 199, 468470. Buikhuisen, M. & Garssen, B. (1990). Hyperventilation and panic attacks. Paper presented at the Tenth International Symposium on Respiratory Psychophysiology, Amsterdam, The Netherlands. Cohen, A., Barlow, D. & Blanchard E. (1985). The psychophysiology of relaxation associated panic attacks. Journal of Abnormal Psychology, 94, 96-101. Comroe, J. H. (1974). Physiology of respiration (2nd edn). Chicago: Yearbook Medical Publishers. Craske, M. & Barlow, D. (1990). Nocturnal Panic: Response to hyperventilation and carbon dioxide challenges. Journal of Abnormal Psychology, 99, 302-307. von Euler. C. & Katz-Salamon, M. (Eds) (1988). Wenner-Gren International Symposium on Respiratory Psychophysiology. London: Macmillan. Fenn. W. 0. & Rahn. H. (Eds) (1964). Handbook of physiology: A critical comprehensive presentation of physiological knowledge and concepts:‘Sec;ion 3: Respiration. Washington;.D.C.: American Physiology- Society. Hibbert, G. & Pilsbury, D. (1988). Hyperventilation in panic attacks: Ambulant monitoring of transcutaneous carbon dioxide. British Journal of Psychiatry, 153, 7680. Lader, M. & Mathews, A. (1970). Physiological changes during spontaneous panic attacks. Journal of Psychosomaric Research, 14, 377-382. Ley, R. (1985a). Agoraphobia, the panic attack, and the hyperventilation syndrome. Behaviour Research and Therapy, 23, 79-8 1. Ley, R. (1985b). Blood, breath, and fears: A hyperventilation theory of panic attacks and agoraphobia. Clinical Psychology Review, 5, 271-285. Ley, R. (1987). Panic disorder and agoraphobia: Fear of fear or fear of the symptoms produced by hyperventilation? Journal of Behavior Therapy and Experimental Psychiatry, 18, 305-316. Ley,.R. (1988a). Panic attacks during relaxation and relaxation-induced anxiety: A hyperventilation interpretation, Journal of Behavior Therapy and Experimental Psychiatry, 19, 253-259. Ley, R. (1988b). Hyperventilation and lactate infusion in the production of panic attacks. Clinical Psychology Review, 8, 1-18. Ley, R. (1989). Dyspneic-fear and catastrophic cognitions in hyperventilatory panic attacks. Behaviour Research and Therapy, 27, 549-554. Mararaf. J.. Ehlers, A. & Roth, W. (1987). Panic attack associated with perceived heart rate acceleration: A case report. Behavior Therapy, 18, 84-89. Pitts. F. & McClure. J. (1967). Lactate metabolism in anxiety neurosis. The New England Journal of Medicine, 277, 132,133,. . Porter, R. (Ed.) (1970). Breathing: Hering-Breuer centenary symposium. London: Churchill. Rachman, S., Levitt, K. & Lopatka, C. (1987). Panic: The links between cognitions and bodily symptoms-I. Behaviour Research and Therapy, 25, 411423. Roth, W. T., Margraf, J., Ehlers, A., Taylor, C. B., Maddock, R. J., Davies S. & Agras, W. S. (1990). Stress test reactivity in panic disorder. Paper presented at the annual meeting of the Society for Psychophysiological Research, Boston, Mass. Sanderson, W. (1987). The influence of perceived control on panic attacks induced via inhalations of 5% CO, enriched air. Unpublished doctoral dissertation, State University of New York at Albany. Sanderson, W. C., Rapee, R. M. & Barlow, D. H. (1988). Panic induction via inhalation of 5.5% CO, enriched air: A single subject analysis of psychological and physiological effects. Behaviour Research and Therapy, 26, 333-335.
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Sanderson, W., Rapee, R. & Barlow, D. (1989). The influence of an illusion of control on panic attacks induced via inhalation of 5.5% carbon dioxide-enriched air. Archives of General Psychiatry, 46, 157-162. Timmons, B. & Ley, R. (Eds) (1992). Behavioral andpsychological approaches to breathing disorders. London: Plenum Press. Wolpe, J. & Rowan, V. C. (1988). Panic disorder: A product of classical conditioning. Behaviour Research and Therapy, 26, 441-450. Woods, S., Charney, D., Goodman, W. & Heninger, G. (1988). Carbon dioxide-induced anxiety: Behavioral, physiologic, and biochemical effects of carbon dioxide in patients with panic disorder and healthy subjects. Archives of General Psychiatry, 45, 43-52.
1992 Copyright
0
THE MANY FACES OF PAN: PSYCHOLOGICAL PHYSIOLOGICAL DIFFERENCES AMONG THREE OF PANIC ATTACKS RONALD
State University
of New York
at Albany,
0005-7967/92 $5.00 + 0.00 1992 Pergamon Press Ltd
AND TYPES
LEY
1400 Washington
Avenue,
Albany,
NY 12222, U.S.A.
(Received 26 March 1991; received for publication IO October 1991) Summary-The thesis of this paper is that failure to recognize the psychological and physiological differences among panic attacks within DSM-IIIR precludes meaningful comparisons and evaluations of research findings, confounds theoretical issues, and impairs the development of more specific, and thereby more effective, programs of treatment. To remedy this, a recommendation is made to define panic attacks on the basis of psychological and physiological distinctions that fit three categories of severity: Type I (classic panic attack), Type II (anticipatory panic attack), and Type III (cognitive panic attack). The logical-empirical rationale for the categories recommended is presented in the context of relevant research findings. Implications for theory, experimental design, and treatment are discussed.
The word ‘panic’ has its origins in frightening tricks played on unwary travelers by the Greek God Pan, a clever and mischievous fellow who frequently used disguises to mask his true identity. Panic disorder as defined by the DSM-IIIR (American Psychiatric Association, 1987) classification covers a rather broad range of symptoms, so broad that the classification may have outlived its usefulness, and may, in fact, be the source of tricks that can confound investigations of the disorder. A few recent studies illustrate problems involved in the identification of the necessary components that define a panic attack. Catastrophic cog&ions. Rachman, Levitt and Lopatka (1987) found that fearful cognitions did not occur in 27% (8 out of 30) of the panic attacks experienced by their sample of panic-disorder patients; and Wolpe and Rowan (1988) found that when they do occur, they follow, rather than precede, the fearful event of the attack. None the less, a cognitive theory of panic attacks (viz. Beck, 1987) rests squarely on the assumption that catastrophic cognitions, which are assumed to be a consequence of the misinterpretation of symptoms, account for the fear experienced in panic attacks. Thus, while catastrophic cognititions rank high among the symptoms of the DSM-IIIR classification of panic attacks, they are not a necessary component of panic. Tuchycardiu. Palpitations and other symptoms of coronary artery disease are frequently reported to occur during panic attacks. However, findings from studies which attempt to induce panic attacks in panic-disorder patients by means of prolonged inhalation of 5% COz in air are not consistent. While Woods, Charney, Goodman and Heninger (1988) report a significant increase in heart rate for patients who experience attacks during inhalation of 5% CO,, Sanderson, Rapee and Barlow (1989) and Craske and Barlow (1990) do not. Paradoxically, in a single-case study in which the S was selected from among those of the Sanderson et al. (1989) sample, Sanderson, Rapee and Barlow (1988) reported a sharp increase in heart rate from 86 to 105 bpm, a finding which is consistent with earlier reports of tachycardia in adventitious panic attacks (i.e. Cohen, Barlow & Blanchard, 1985; Margraf, Ehlers & Roth, 1987; Lader & Mathews, 1970). Since tachycardia is not common to all panic attacks induced by the 5% CO, challenge, this frequently reported symptom of the DSM-IIIR classification appears not to be a necessary component of panic. Hyperventilation. Although Ley (1985b, 1989) has placed heavy emphasis on the central role of the sequelae of hyperventilation in the producton of dyspneic-fear and the common symptoms of panic attacks, Hibbert and Pilsbury (1988) reported a test trial of transcutaneous monitoring of pC0, in which one of four patients who claimed to have a panic attack did not show a concurrent decrease in pC0,. Although almost all the symptoms of panic listed in the DSM-IIIR classification are common effects that can be produced by hyperventilation, it appears that hyperventilation may not be a necessary component of panic. Furthermore, since prolonged inhalation of 5% CO, 347
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precludes the possibility of hypocapnea, panic attacks reported during such inhalations cannot be the result of hyperventilation. DSM-IIIR
and the dejinition of panic
Although the DSM-IIIR classification reflects research findings which make it clear that the sudden onset of intense fear, dyspnea, tachycardia, and catastrophic cognitions are among the most common symptoms of panic attacks, the classification does not specify which symptoms, if any, are essential components that define the panic attack. If there are no essential components and if we accept Beitman, Basha, Flaker, DeRosear, Mukerji and Lamberti’s (1987) contention that there are panic attacks without fear, then a patient who presents, for example, ‘trembling’, ‘hot flushes’, ‘sweating’, and ‘feelings of unreality’ (four symptoms of DSM-IIIR) in association with episodes of intense ‘discomfort’, could be diagnosed as suffering panic disorder (given the necessary frequency and recency of such episodes), though there is no fear, no dyspnea, no tachycardia, and no catastrophic cognitions. While some critics of DSM-IIIR might argue that such a diagnosis would be absurd because it strips ‘panic’ of its basic meaning, the diagnosis in question might be defined by others as a logically valid conclusion. Is it possible to resolve the conflict between the charge of absurdity and the retention of the primary features of the DSM-IIIR, and at the same time find accommodation for the validity of the research findings cited above? The present paper addresses this multi-faceted question and offers an answer in terms of a refined classification of panic attacks. A Panic Attack is not a Panic Attack is not a Panic Attack The identification of the necessary components of panic is, in a sense, part of the theoretical problem, a situation which is bound to breed chaos because conflicting theoretical interpretations cannot be compared and evaluated if they are addressed to different, albeit similar, phenomena. The purpose of the present paper is to describe three distinctly different types of panic attacks, all of which meet the criteria required by the DSM-IIIR classification. The importance of making the distinctions recommended here lies in the clarification of theoretical issues, the facilitation of communication in research, and the development of effective programs of treatment through greater specificity of the underlying complaint. While the categories offered may not exhaust all of the possible types of panic attacks that might fall beneath the DSM-IIIR heading, they are intended to cover the major varieties of attacks discussed in the contemporary professional journals that publish articles dealing with theory and treatment of panic disorder. The idea that there may be more than one type of panic attack is not new: Ley (1987) and Wolpe and Rowan (1988) proposed that panic attacks can be described in terms of a Pavlovian Table I. Psychological/subjective
and physiological/objective
Psychologicol/subjeclive
dis~inclions
(probabiliry
and expected
inlensify)
Fear
terror (extreme dyspneic-fear) with desire to flee
(2)
Dyspnea (difficulty breathing, air hungry, choking, smothering) Palpitations Catastrophic Cognitions
p-high (sense suffocation)
Remaining IIIR
p-high
(5)
Physiological/objecfioe (6)
(7) (8) (9)
symptoms
among three types of panic attacks Type III (Cognitive PA)
(1)
(3) (4)
distinctions
Type II (Anticiuatorv PA)
Type I (Classic PA)
p-high vhigh thoughts)
of DSM-
distinctions
(+
=present,
in drop Sharp PC01 > IO mmHg Sharp increase in respiration rate and/or tidal volume Sharp increase in heart rate > 10 bpm Sharp increase in clectrodermal response
-
of
(‘unreal’
impending
or
bizarre
fear or anticipatory anxiety (strong dread of what may folIOW) p-medium
apprehensive
p-medium *medium (fearful thoughts but not in context of ‘unreality’)
@OW @ow (mundane ful thoughts)
pmedium
p-IOW
= not presenl)
anxiety
p-&W
+
-
+
-
+
_
+
-
4.
-
_
fear-
Three types of panic attacks
349
conditioning paradigm in which a primary hyperventilatory panic attack constitutes the unconditioned response, and a secondary anticipatory attack constitutes the conditioned response. While the present proposal is an outgrowth of this point of view, the categories presented here do not require the assumption of a Pavlovian conditio~ng paradigm. Types of Panic Attacks The classification of panic attacks in terms of three types is based on two sets of criteria: psychological/subjective distinctions and physiological/objective distinctions. Table 1 lists five psychological criteria and five physiological criteria upon which distinctions among the three types of panic attacks are made. Case reports that exemplify each type are given below. Classic panic attack The psychological/subjective distinctions that mark the Type I or classic panic attack were derived from analyses of studies that measured the frequency and intensity of symptoms reported to occur during panic attacks (e.g. Barlow, Vermilyea, Blanchard, Vermilyea, DiNardo Br Cerny, 1985; Ley, 1985a,b; Rachman, Levitt & Lopatka, 1987) and from collateral studies of dyspneic complaints in breathing disorders (e.g. Comroe, 1974; Fenn & Rahn, 1964; Porter, 1970; Timmons & Ley, 1992; von Euler & Katz-Salamon, 1988). The significance and centrality of seemingly uncontrollable dyspnea in conjunction with fear in Type I panic attacks is clear (Ley, 1989; Rachman er al., 1987). As Aiken, Zeally and Rosenthal (1970) have pointed out: Dyspnea may be felt as endangering to life to a greater extent than almost any other symptom: to the patient, the experience of dyspnea is regarded as something which, if it worsens, to asphyxia must inevitably be fatal (p. 256). The Type I panic attack is marked by uncontrolled, high-intensity dyspnea (sense of impending suffocation) and heart palpitations accompanied by terror (extreme dyspneic-fear) together with a strong desire to flee. The catastrophic cognitions that often follow are marked by thoughts associated with death or impending doom. Compared with the Type II and Type III panic attacks, the probability and intensity of experiencing the remaining symptoms of the DSM-IIIR classification are highest. The physiological/objective distinctions that mark the Type I panic attack were derived primarily from analyses of adventitious panic attacks that occurred in a laboratory setting during physiological assessments (Cohen et al., 1985; Lader & Mathews, 1970) or during the administration of treatments in experimental research (Margraf et al., 1987; Sanderson, 1987). The most complete physiological description of a Type I panic attack can be found in a single-case study by Sanderson et al. (1988) based on data all of which came from a single S selected from an earlier experiment by Sanderson (1987). In this earlier experiment, Sanderson required a panic-disorder patient to breathe room air via an inhalation mask during a 5 min baseline period prior to a scheduled 20 min period during which the patient was told that she would be breathing a gas which might produce a panic attack. After 6 min of inhalation of room air (the gas the patient believed could produce a panic attack, i.e. the ‘panic-induction gas’) a panic attack was reported: anxiety increased sharply (Fig. I), heart rate increased from 86 to 105 bpm (Fig. 2), electrodermal response showed a sharp increase in conductivity (Fig. 3), respiration rate increased (Fig. 4), and end-tidal pCO,, which was constant throughout the entire procedure (mean pCOz = 24.5 mmHg, SD = 0.67), fell precipitously from 26 mmHg during the next-to-final minute to 17 mmHg during the final minute when the patient reported a panic attack (Fig. 5). Except for low finger temperature, an effect that was observed during an adventitious panic attack reported by Cohen et al. (1985), all of the physiological markers of a Type I panic attack listed in Table 1 were presented by the patient. Case of a Type I panic attack The following abstract from illustrates the extreme severity cognitive impai~ent, as well experienced. The patient was a
an interview with a panic-disorder patient was selected because it of a Type I panic attack in terms of behavior and evidence of as an intros~tive report of fear and the dominant symptoms 3S-yr-old woman who experienced a panic attack while driving to
3.50
RONALD LEY
8
“Panic-Induction” Air
6
I
Pre
7.5
Minutes
10.0
11.0
&Port Panic
Fig. I. Subjective anxiety ratings during baseline air and panic-induction air. Adapted from Sanderson et n!., 1988.
her home in a suburb of Albany, N.Y. during the first cold and snowy night of winter. She reported that her heart suddenly began to beat wildly as she struggled to breathe. Although she was driving on a dark country highway with no help in sight, she stopped her car in the middle of the road, got out, and started running down the highway. She did not know where she was going or what was happening to her, but that she felt that she was going to die and that she had to leave the car and run away. Her recall of events that followed was vague, but she remembered that it was a truck driver who found her and took her to the emergency room of a local hospital. Anticipatory panic attack
The psychological/subjective distinctions that mark the Type II or anticipatory panic attack were also derived from analyses of studies that measured the frequency and intensity of symptoms reported to occur during panic attacks, especially studies that used prolonged inhalation of 5% CO, as an aversive challenge for provocation of panic attacks (e.g. Craske & Barlow, 1990; Roth, Margraf, Ehlers, Taylor, Maddock, Davies & Agras, 1990; Sanderson et al., 1989; Woods et al., 1988). The C~*-challenge studies provide a unique opportunity to study the occurrence of Type II panic attacks because in addition to meeting the criteria listed in Table 1, inhalation of 5% CO2 in room air precludes the possibility of hyperventilation and its hypocapneic psychological and physiological sequelae. An examination of the fear or anxiety ratings of those Ss who are reported to experience panic attacks during prolonged inhalation of 5% CO2 makes it clear that the intensity of fear reported is significantly less than that experienced during panic attacks in the everyday world (see Craske & Barlow, 1990; Woods et al., 1988) and that the focus of fearful concern is centered on what might happen (i.e. anticipations rather than what is happening. Furthe~ore, the qualitative analysis of panic attacks during inhalation of 5% CO2 makes it equally clear that the terror and desire to flee
351
Three types of panic attacks “Panic-Induction” Air
A
85
80
I
I
I
I
I
I
6
7
8
9
10
11
Minutes
P&c
Fig. 2. Mean heart rate for five I-min periods during baseline air (l-5) and six I-min periods during panic-induction air (6-I 1). Adapted from Sanderson et al., 1988.
that characterize the Type I panic attack are not reported during panic attacks induced by 5% CO*: Roth et al. (1990) reported that of 24 patients who experienced panic attacks during inhalation of 5% CO*, 10 (42%) did not request that the administration of the gas be discontinued While it is highly likely that the occurrence of a panic attack in the relative safety of the laboratory attenuates the intensity of the fear experienced (Ley, 1988b), a comparison of the subjective reports of patients who experienced attacks induced by lactate infusion (e.g. Bonn, Harrison & Rees, 1971; Pitts 8z McClure, 1967) with those of patients whose attacks were induced during inhalation of 5% CO, suggests that factors other than the safety of the laboratory account for the relative diminution in intensity of attacks during inhalation of 5% CO,. As for the symptoms of the DSM-IIIR classification of panic, studies that use the 5% CO, challenge, report lower frequencies and/or lower intensities and/or lower similarity ratings compared with those experienced during panic attacks in the everyday world. Sanderson (1987), for example, compared both the frequency and intensity of 16 symptoms of DSM-IIIR reported by patients during panic attacks induced by 5.5% CO, with the frequency and intensity of symptoms during panic attacks in the natural environment and found the following: Frequency of symptoms. Excluding the sensation of ‘panic or fear’, which was reported by all Ss, Sanderson (1987) found that only three of 15 symptoms (binomial P -c 0.01) were identified to have occurred more frequently during the CO, induced panic attacks: ‘pounding or racing heart’, ‘breathlessness or smothering sensations’, and ‘choking’. It should be noted, in connection with these symptoms, that while prolonged inhalation of 5.5% CO2 will increase ventilation dramatically (minute volume will be increased about threefold) and give rise to dyspnea (especially if Ss attempt to retard breathing by slowing down respiration rate), Sanderson found virtually no increase in heart rate from baseline (M = 82 bpm) to, and throughout, a 15-min period of prolonged inhalation of 5.5% CO, (M = 83 bpm).
352
RONALD LEY
-3.5
“Panic-Induction” Air
Air
-3.0 F
-1.0
s
-0.5
d 8
BL .5
I
I
I
I
6
7
8
9
I
I
10 11 Report Panic
Fig. 3. GSR (J&) changes for five I-min periods during baseline air (i-5) and six I-min periods during panic-induction air (a-1 1). Adapted from Sanderson ef al., 1988.
Intensify of symptoms. Sanderson’s (1987) intensity ratings of symptoms on a scale of l-8 (1 = slightly felt, 8 = very strongly felt) showed an even more remarkable pattern. Except for ‘nausea or abdominal distress’ (5.7 during CO* panic, 5.3 during natural panic), all of the intensity ratings were less during panic attacks induced by 5.5% COz than those during panic attacks in the natural environment, including ‘panic or fear’ (5.4 during COz panic, 7.5 during natural panic). ~fmilarify ratings. While Sanderson’s findings pertaining to differences in the frequency and intensity of symptoms point indirectly to the relatively low similarity between naturally occurring panic attacks and those induced by 5.5% CO*, Craske and Barlow (1990) provide direct evidence of the low similarity. On a nine-point scale (0 = not at all similar, 8 = identical) of similarity of ‘symptoms and feelings to naturally occurring fear/panic reactions’, one group of panic disorder patients (n = 16) gave a mean rating of 3.0 to the similarity of their experiences during a 15 min period of prolonged inhalation of 5.5% CO,, while the other group (n = 18) gave a rating of 3.9. The physiological/objective distinctions that mark the Type II panic attack are limited to occasional sharp increases in heart rate and electrodermal conductivity. Regarding heart rate changes, for example, a more detailed examination of the results of Woods et al. (1988) reveals that the mean heart rate change for all of the 14 patients who breathed 5% CO, increased significantly from baseline by 16 bpm, and for the eight patients who panicked, heart rate increased by 25 bpm. Sanderson (1987), on the other hand, reported no increase in heart rate for patients who panicked and patients who did not. The findings of Craske and Barlow (1990) are also inconsistent with those of Woods et al., but in agreement with those of Sanderson (1987). That is, for a group of 16 panic-disorder patients, Craske and Barlow reported that heart rate at baseline (77.4 bpm, SD = 11.7) was identical with heart rate during inhalation of 5.5% CO2 (77.4, SD = 11.8). Furthermore, for a second group of 18 patients, heart rate at baseline (75.8 bpm) deviated ever so slightly from heart rate during inhalation of 5.5% CO2 (76.0 bpm). Some place
Three types of panic attacks
353
17
16
13
12 Air
“Panic-Induction”
Air
Fig. 4. Mean respiration rate (bpm) for five I-min periods during baseline air (1-5) and six 1-min periods during panic-induction air (6-11). Adapted from Sanderson Ed al., 1988.
in between the extremes of the findings of Woods et al. (1988) and those of Sanderson (1987) and Craske and Barlow (1990), Roth et al. (1990) reported essentially the same small increase in heart rate of approx. 5 bpm for all patients (panickers and nonpanickers alike) and normals from baseline to the period of inhalation of 5% C02. While other physiological indices might show changes in the same direction as those that occur during Type I panic attacks, such changes would not be expected to show consistently the same sharp changes of equal magnitude to those that occur during Type I attacks. A comparison of the findings of Roth et al. with the case studies that illustrate the Type I attack (i.e. Lader & Mathews, 1970; Sanderson et al., 1988) makes this clear. A caveat to be noted in connection with prolonged inhalation of 5% CO, is that such inhalations can lead to a Type I panic attack if the increased ventilation stimulated by the CO2 continues after the termination of the CO*. That is, while the hyperpnea induced by 5% CO, is protected against the production of respiratory alkalosis, prolonged hyperpnea following 5% CO, is not. Therefore, a patient subjected to prolonged inhalation of 5% CO2 is vulnerable to a Type I panic attack in the period immediately following termination of CO,, especially if the assessment procedure immobilizes the S therby restricting the metabolic production of CO, (see Ley, 1988a). Although research findings from analogue studies of the effects of prolonged inhalation of 5% CO, provide data relevant to Type II panic attacks, there is no environment outside the laboratory where air contains 5% CO,. What then accounts for Type II panic attacks in the everyday world? As indicated earlier, the occurrence of Type II attacks can be explained on the basis of Pavlovian conditioning (Ley, 1987; Wolpe & Rowan, 1988). From this point of view, the conditioned stimulus (CS) consists of signals which predict the probable onset of an unconditioned stimulus (UCS) that consists of hyperventilatory hypocapnea or any event that gives rise to severe uncontrollable dyspnea with concomitant dyspneic-fear (UCR-unconditioned response); the conditioned
RONALD LEY
354
“Panic-Induction” Ah
Air 26
25
h 24-
23 -
19 18 -
“12
3
4
5
6
Minutes
7
8
9
10 11 Report Panic
Fig. 5. Mean end-tidal pC0, in mmHg for five I-mm periods during baseline air (l-5) and six I-min periods during panic-induction air (611). Adapted from “The influence of perceived control on panic attacks induced via inhalations of 5% CO, enriched air”, by W. C. Sanderson, 1987, unpublished doctoral dissertation, State University of New York at Albany.
response (CR) consists of fear without dyspnea (anticipatory anxiety) that occurs in response to the CS. While Type II panic attacks might be explained from other points of view, two distinctive implications of a Pavlovian conditioning interpretation should be noted. One is that Type II panic attacks must be preceded by a history of at least one Type I attack. The other is that a Type II panic attack could progress into a Type I attack if the anticipatory anxiety is sufficiently prolonged and/or sufficiently intense to produce the degree of hypocapnea necessary for the induction of severe uncontrollable dyspnea. Case of a Type II panic attack The following abstract illustrates the moderate severity and type of symptoms often reported by a panic-disorder patient during panic attacks induced by prolonged inhalation of 5% CO2 in air. The patient was a young adult woman with a 2 yr history of panic attacks. She reported an attack during inhalation of 5% CO1 in air: (a) mild dyspnea, (b) mild palpitations, (c) weakness, (d) fear of losing control, (e) dread of what might follow. The patient was told before administration of 5% CO* that the gas would increase her ventilation and might produce a panic attack. Cognitive panic attack
The psychological/subjective distinctions that mark the Type III or cognitive panic attack include a relatively mild state of apprehension associated with timidity and lack of assertiveness, in which the terror and strong desire to flee that marks the Type I attack and the anticipatory anxiety (strong dread of what may follow) that mark the Type II attack are missing. The underlying anxiety of the Type III panic attack is probably generated by worry and excessive concern with real, but relatively minor, negative events or major negative events for which the probabilities are low, e.g.
Three types of panic attacks
355
“What will happen to me if my car breaks down when I am alone? What will my parents think of me if I get low grades in school? How would my family get on without me if I died in an airplane crash?” Unlike the Type I panic attack in which the symptoms precede the onset of terror, the Type III attack is marked by occasions in which a relatively low level of chronic anxiety waxes and leads to an increase in arousal which produces symptoms of anxiety which are sufficiently strong to alarm the sufferer, who often makes a catastrophic interpretation of what the symptoms signal. In the case of Type III panic attacks, the anxiety precedes the symptoms. Such increases in anxiety that trigger Type III panic attacks are probably the consequences of a relatively stressful event which cannot be conveniently avoided; e.g. being called on to recite in class, having a flat tyre or accident while driving alone, receiving an anonymous harassing phone call. While a relatively large number of symptoms of DSM-IIIR may be identified by the patient, a careful analysis will typically reveal that the intensity of such symptoms is low compared with those reported to occur during Type I and Type II attacks. The physiological/objective distinctions that mark the Type III panic attack are the absence of any significant changes in functions indicated by the five criteria of Table 1, or, at best, slight manifestations of the symptoms when provoked by thoughts that center on the patient’s primary sources of anxiety. Type III panic attacks reported during physiological assessments will show small or no correlated changes in physiological functions such as breathing and heart rate. Patients identified as sufferers of Type III panic attacks will not be discernible from asymptomatic Ss on standard psychophysiological assessment measures (Bruce Cuthbert and Peter Lang, pers. commun., 18 October 1990), and panic attacks reported during ambulatory monitoring will show little or no correlated change in the physiological variables monitored (e.g. Buikhuisen & Garssen, 1990). Case of Type III panic attack
The follo~ng abstract from an interview with a panic-disorder patient was selected because it illustrates the relatively mild severity of a Type III panic attack in the everyday world. The patient was a passive young adult woman with a 6 yr history of panic attacks that began in a college classroom in a course with an instructor who frightened her because he had a reputation as a ‘hard marker’; the patient was afraid that she might get a low grade and lose her father’s approval. She claimed to have a panic attack during every class period, but remained in her seat and did not leave the classroom until the class was over. She did not miss a single class for the entire semester for fear that it might jeopardize her grade. Her panic attacks were marked by anxiety and most of the other symptoms listed in DSM-III classification, except that she reported that most of the symptoms followed, rather than preceded, the onset of her attacks. DISCUSSION
Theory and research
The implications of the proposed refinement in the definition of panic attack for theory and research are clear. The resolution of some theoretical conflicts among current explanations of panic (e.g. Barlow’s interoceptive conditioning fear-of-fear hypothesis, 1987; Beck’s cognitive-misinterpretation-of-symptoms model, 1987; Ley’s hyperventilation theory, 1985b, 1989) may be found if the results of studies in the future are analyzed in terms of the three types of panic attacks proposed here. That is, conflicting research findings and conflicting theoretical positions based on such findings may be the consequence of critical differences among Ss all of whom are identified as patients suffering panic attacks as defined by DSM-IIIR. Even if the approach proposed here does not resolve conflicting theoretical issues, nothing would be lost, and perhaps greater experimental precision would be gained through increasing the homogenity of experimental groups and thus reducing Beta errors, the bane of the research scientist. That is, the present proposal offers a possible means for improving research designs for the study of panic disorder by providing a basis for increasing statistical precision (i.e. reducing within-group variance) through blocking on the three types of panic and by providing the basis for the determination of interactions among the three types of panic and other experimental treatments or characteristics of the Ss.
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Treatment Unlike some psychotherapeutic approaches in which all complaints receive the same treatment, behavior therapy is based on the assumption that the remedy must be designed to fit the complaint. In the case of panic disorder, differences in treatment and differences in the relative success of treatment may depend to some extent on differences among patients with respect to the three types of panic attacks outlined here. Clearly, breathing retraining would be expected to be most beneficial to patients who suffer Type I attacks, while cognitive approaches would be expected to have the most benefit for those who suffer Type III attacks. Issues of the most efficacious approach aside, keener distinctions among the underlying complaints of patients will lead to improved techniques of treatment and thus deliver the greatest benefits to patients. Although the Greek God Pan often wore disguises that aided him in his cruel and mischievous behavior, he was a safeguard for those who believed in him, for those who saw him for what he was-a complex and many-sided figure.
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Three types of panic attacks
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