Introduction
According to the 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 and at least four of the 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” (Burns 2006, p. 76).
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” (Burns 2006, p. 77). 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 (American Psychiatric Association, 1987),
Main body
The Manual specifies that an organic etiology is excluded as a cause of these manifestations, and the disturbance must persist for at least I month beyond the cessation of any precipitating organic factor. DSM–III–R also states that the attack must be
- unexpected, that is, not occur immediately before or on exposure to a situation that almost always caused anxiety, and
- 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 (Barlow, D.H. et al., 1994). The DSM–III–R conception of panic disorder is strongly influenced by Klein’s approach, which has been to categorize symptoms into syndromes (Klein, 1993). Some of the researchers (Carr & Sheenan, 1998) 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.
Among the differing theories that have been proposed, some of the recent biological theorists posit that panic disorder is a discrete psychiatric syndrome stemming from an inherited neuro-chemical disease (Carr & Sheehan, 1998). Most researchers use either a biological approach, aimed at understanding the neurophysiological basis of panic, or a cognitive-behavioral approach, aimed at understanding psychological mechanisms of panic and its consequences. The model of panic disorder is an integrated one, drawn from the paradigm used by investigators in the field of psychosomatic medicine. This approach uses a biological conception of panic, as a disturbance of brain function.
The principles of psychosomatic medicine are based on a view of health and disease which includes the effects of psychophysiological reactivity on organic function. Psychological factors are seen as important mediators of physiological changes and vice versa. Social relationships and environmental events are taken into account since such events influence mental and bodily function. Psychosocial input probably acts via neurohormonal mechanisms regulated by the central nervous system, and has both immediate and long-term effects on the central nervous system. In the psychosomatic paradigm, symptomatic illness represents a final common pathway of a variable series of interacting psychological and biological disturbances (Carr & Sheenan, 1998).
Panic is well described in both the lay and scientific literature. The dictionary (McNally 1994, p. 82) definition, “sudden overpowering fright” or “sudden unreasoning terror often associated with mass flight” captures the core descriptive characteristics:
- intense fear,
- sudden onset,
- a sense of being overpowered or out of control,
- loss of reasoning capacity and
- a strong urge to flee.
Panic can be conceptualized as an emergency biobehavioral response to situations of catastrophic and immediate threat (Nunn, 1998). As such, panic includes a cognitive appraisal of danger accompanied by physiological and behavioral activation. Panic is also an affective state related to anxiety and possibly depression. Physical sensations are prominent and include heart palpitations, shortness of breath, sweating, trembling, weakness, dizziness, nausea and diarrhea (Nunn, 1998).
Panic is considered as a normal response to conditions where coping ability are overwhelmed influenced by the feelings of fear and danger. The individual utilizes last-ditch, emergency trying to cope with fear and terror which are automatic and difficult to control. These reactions force an individual to search for safety and help. If a person cannot find or see the possible way out, it can lead to such reactions as freezing or aggressive behavior (Nunn, 1998).
Panic is described as a reaction towards danger and organism’s total commitment to escape the danger or unpleasant situation. It is possible to imagine a scenario where such a response would be adaptive: If primitive man or woman chanced upon a watering hole frequented by a group of panthers, a single, close encounter with one of the beasts could lead to a panic episode facilitating quick escape and future avoidance of the watering hole (McNally & Foa, 1987).
Donald Klein (1993) can be credited with the identification of panic as a discrete psychopathological symptom. Full-blown panic attacks are distinguished from limited symptom episodes by intensity and number of symptoms. In many studies, and in the revision of DSM-III, full-blown panic is defined as consisting or four or more symptoms from the DSM-III list, while partial panic (also called near-panic, limited symptom attacks, or subpanic) has fewer than four (Nunn, 1998).
Full-blown panic is usually longer in duration and/or higher in intensity than partial panic. Sudden onset and rapid peak differentiates panic from generalized anxiety, and lack of triggers differentiates panic from phobic anxiety. In the biological model, panic is conceptualized as resulting from excessive firing of the central nervous system, which regulates the biobehavioral expression of fear and its associated somatic symptoms.
Panic attacks are viewed as analogous to a seizure disorder in which the threshold for neuronal firing is abnormally lowered. Noradrenergic, adrenergic, benzodiazepine, serotonin, and adenosine receptors have been postulated to have a role in panicogenesis. Neurotransmitter abnormalities may reflect defects in synthesis, release, degradation, or receptor function. These abnormalities may be due to changes in intracellular processes, membrane physiology, or extracellular microenvironment (e.g., ionic gradient, hormonal constitution, metabolical state).
Studies are in progress to try to tease apart these various alternatives (Kolb & Fantie, 1998). The “false suffocation alarm” hypothesis introduced by Klein (1993) suggests that panic is caused by simultaneous dysfunction of neurotransmitter systems (Coplan, J.D. & Lydiard, R.B., 1998).
The cognitive-behavioral model is different from the biological model in that panic is seen as a manifestation of sudden, intense anxiety and/or fear. Panic attacks are always cued by a frightening situation, though the content of the fear may be out of awareness. Panic occurs in all anxiety disorders and may or may not warrant a separate diagnostic category. The states of fear, anxiety, and panic are triggered in reaction to appraisal of danger.
Appraisal of danger is a subjective matter which involves simultaneous processing of threat and safety information. In other words an identified danger situation can be conceptualized as the net result of appraisal of degree of external threat, and effectiveness of protective mechanisms (McNally, 1995). In normal individuals, the presence of a severe external threat in an unsafe setting can trigger panic. A fire (serious threat) in a crowded theater (an unsafe setting) is an example. Intriguing recent research (Rachman et al 1987) suggests that normal individuals may also experience occasional panic attacks in the absence of external threat.
Panic disorder patients regularly have panic attacks in the absence of external threat. The cognitive model holds that these patients have abnormal cognitive processes which lead them to perceive threats in the absence of an actually threatening situation. Research efforts are directed at trying to identify which cognitive processes are involved. There is some evidence that panic patients feel themselves to be unsafe in ordinary situations.
Panic patients may be preoccupied with ideas of catastrophic personal or social harm, from which they feel helpless to protect themselves. In this setting, they are likely to misconstrue small changes in bodily sensations as indicative of life threatening illness, loss of consciousness, or going crazy. Once a panic episode has occurred, further panics may be triggered in response to associated cues by a mechanism of classical conditioning. Operant conditioning may also increase panic susceptibility after successful reduction of panic sensations through escape (Abramson et al 1978).
The treatment implications following from the biological theories, obviously, mostly involve medications. Pharmacological treatment studies reveal good antipanic efficacy of imipramine, desipramine, phenelzine, and alprazolam. Standard benzodiazepines are often helpful to panic patients, but do not appear to block panic with the same degree of efficacy as the newer triazoiobenzodiazepines, tricyclic antidepressants, or monamine oxidase inhibitors.
Beta adrenergic blocking agents have been used, but are not generally effective in treating panic. The alpha-adrenergic agonist, appears to be effective initially, but may lose antipanic efficacy with continued use (Barlow, 1998). Pharmacological studies to date have not elucidated pathophysiological mechanisms and they propose two main reasons to explain this failure. First, etiological heterogeneity may mean that large samples are needed to dissect subgroups with specific pharamacological responsiveness (Barlow & Craske 1993). Second, there is a need for a systems model of pathology to replace the rheostat model often used.
This means that pathogenesis may relate to abnormal feedback circuits or changes in the character of neural responses, rather than to rheostatic changes in transmitter release or receptor sensitivity. It is also possible that the best model of panic requires consideration of multiple, interacting neurophysiological systems (Barlow et al 1994).
In the case of attacks which are preceded by heightened anxiety, two distinct types of attack can be distinguished. In the first, the heightened anxiety is concerned with the anticipation of an attack. Individuals who have recurrent panic attacks have a tendency to misinterpret bodily sensations even when they are not anxious, it is not clear whether this “trait” antedates the first panic attack. It could be that in some individuals adverse life events (a relative dying suddenly and unexpectedly) may produce a tendency to misinterpret bodily sensations before the first attack occurs (Barlow et al 1994).
First, the simple statement that panic results from a fear of fear would lead one to predict that panic patients would always panic when they notice themselves becoming anxious. This is clearly not the case. There are many occasions in which panic patients notice that they are fairly severely anxious but do not panic. For example, a patient who experiences panic attacks may notice that he or she is becoming anxious before an interview but not panic.
Instead the patient may simply ascribe the bodily sensations being experienced to the understandable apprehension produced by a difficult situation. The cognitive model avoids the problem of overprediction by specifying that individuals only panic when they notice themselves becoming anxious if they interpret the bodily symptoms of anxiety as indicating an immediately impending disaster. The experimental evidence most relevant to this issue comes from studies investigating the effect of cognitive set on response to biological inductions.
Normal subjects, given a negative interpretation of the bodily sensations resulting from hyperventilation, reported that this was a more unpleasant experience than subjects given a positive interpretation (Clark, 1986).
Cognitive theorists also examine locus of control in patients with panic disorder. Locus of control is generally felt to represent the extend to which an individual perceives personal control over events in one’s environment (Otto, Pollack, Penava & Zucker, 1999). Agoraphobics scored as more external on Rotter’s locus of control scale. Since depression is a common feature of agoraphobia and was not taken into account in the analyses, interpretation of these data is problematical. Attribution was also examined after subjects were exposed to manipulated failure or success on an anagram-solving task. Few differences were observed between subject groups (Clark, 1988).
Agoraphobics in the failure condition were found to rate their performance as more personally significant and as having more impact on other areas of their lives. Agoraphobics perceived the internal causes of negative events as more consistently present, more important, and as influencing more life situations. Because depression scores were higher among agoraphobics, and this difference was not considered in data analyses, it is once again difficult to interpret these data (Coplan & Lydiard 1998).
Attributional styles were introduced by Abramson, Seligman and Teasdale (1978), who stated that the individual’s attributions can be seen as causes of positive and negative events. All records had been obtained without reference to the study. These written records were scored blindly for attributional patterns with a content analysis system (Clark, 1993). The characteristic attributional style for depression (perceiving negative events to be global, stable, and internal in cause) was found for the depressed but not for the clients.
These findings indicate that attributional styles among the neurotic disorders differ. On the whole, these studies indicate that when anxiety is mixed with depression, some elements of the depressive attributional style are found, albeit inconsistently (Abramson et al 1978). Castellon and Riskind’s study suggests that if depression had been controlled in other studies, this style would not have been found among anxious patients. This is not an important point for the clinical picture, which is typically mixed. Not making this distinction does confound our efforts to arrive at a theoretical understanding of anxiety. A characteristic attributional style for anxiety has yet to be identified.
While the focus on behavior has been salutary, the limitations of traditional conditioning theory in explaining complex pathologies have become increasingly apparent. The method of cognitive behavior therapy and analysis is an effort to respond to this problem. In some ways this approach has represented a step backwards, as it revived the subjective conception of behavioral causality (Rosenzeweig et al 2005).
Furthermore, until very recently, the cognitive-behavioral approach has ignored a major “second revolution” in experimental psychology, based on a wholly new way of comprehending mentation, which is geared to the complexity of human behavior and potentially free of phenomenological bias. It is this novel, third way of explaining intentional systems that is the focus of this presentation. This behavioral revolution focused research on the field of conditioning, which culminated in the development of potent behavioral methods for the analysis and treatment of anxiety disorders (Abramson et al 1978).
The focus is on how the brain processes images. In the present context, images are considered to be perceptual-motor information structures. They are memory structures which integrate environmental inputs, semantic information, and action patterns, and are the cognitive format of effective expression. It is argued that image processing and/or the organization of emotional memories differ significantly among anxiety disordered patients.
The primary goal of the subsequent theoretical presentation and research description is to elucidate these differences–to help develop a more parsimonious foundation view for the cognitive analysis of anxiety disorder, including panic states (Rosenzeweig et al 2005). It is proposed that emotional responses be construed primitively as action dispositions, that is, efferent programs which mobilize the organism for flight and attack. In less complex animals, and for the most part in humans, emotional behavior is context bound. In Pavlovian theory, a conditioned stimulus, for example, a kitten is paired in time with a traumatic unconditioned stimulus, like being bitten, which produces an unconditioned response, fright. Later, seeing cats produces the conditioned response of fear, and avoidance results.
Here, Pavlovian theory postulates a spontaneous panic. The Pavlovian account is parsimonious, rooted in behavioral science, and well tested in its general propositions, but not in this manifestation. In addition, like the cognitive account, it subsumes the biological data by the parallel moves. The effects of therapeutic drugs are explained by claiming elimination of either the conditioned stimulus of bodily sensations.
A Pavlovian explanation claims that the effect of information and interpretation is merely to make the extinction trials more salient or effective. That panic disordered patients will interpret bodily sensations more negatively than other anxiety disorder patients; that drugs produce panic by producing bodily sensations of panic; and that treatments that change interpretations of bodily sensations will do better than treatments that do not). The influence of safety signals on the cognitive consequences of panic is implicit in much of cognitive therapeutic procedures, but has yet to be analyzed systematically. At this early stage, a most interesting question is why the provision of safety information appears to require validating confirmation by behavioral rehearsal (Carr & Sheehan, 1998).
The biological approach can cope with such evidence, simply by dismissing it as irrelevant, as follows: It is interesting, but hardly surprising, that it is possible to show experimentally that cognitive set can modify the affective reaction to induced bodily sensations, but this evidence is quite irrelevant to the etiology of spontaneously occurring panic attacks (Carr & Sheehan, 1998). Thus, again, evidence under this head, while consistent with the cognitive model, can also be accommodated within the more biological account.
The cognitive and more biological accounts make clearly different predictions concerning the effects of reducing the tendency to make catastrophic interpretations of naturally occurring bodily sensations. As far as the cognitive model is concerned, reducing this tendency will eliminate the key element in the escalation of panic, and so the frequency of panic attacks should be drastically reduced. According to Clark (1993), catastrophic misinterpretations need not to be conscious to trigger a panic attack “ in patients who experience recurrent attacks, catastrophic misinterpretations may be so fast and automatic that patients may not always be aware of the interpretive process” (p. 76).
As far as the more biological account is concerned, such interpretations are epiphenomenal and so modifying them should have little effect on frequency of panic attacks. The necessary evidence on this issue would be provided by evaluating the effects of interventions that modify catastrophic interpretations without also affecting other factors that could plausibly account for any beneficial effects observed. Evidence for the effects of cognitively targeted treatments will be reviewed in detail later.
The pattern of fearful cognitions and of accompanying bodily sensations reported on these no-panic trials resembles the pattern on panic trials. It remains possible that the differences between panic and no-panic trials are those of intensity, but at present, we are not in a position to explain the non-occurrence of panics in these instances (Carr & Sheehan, 1998).
Conclusion
The consequences of panic often take the form of avoidance behavior but there are important exceptions. Avoidance can develop after non-panic experiences, panics are reported by patients who do not display avoidance, and panics are reported by nonpatient samples who do not display avoidance behavior. In sum, panic and avoidance often are connected but panics can occur without avoidance emerging, and avoidance can occur without panics. The facts and theories analyzed above show that there no a unified and single theory concerning etiology and maintenance of panic disorder. Each of the models provide researchers with unique interpretations of panic disorders but all of them have some limitations and drawbacks.
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