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issues that remain unresolved. First, there is evidence that catastrophic misinterpreta-
tions of bodily sensations may not be necessary to experience a panic attack, a finding
that directly challenges a major tenet of the catastrophic cognition model of D. M.
Clark (1988). (For further discussion of this criticism, see Hofmann, 2004a; McNally,
1994; Rachman, 2004; Roth et al., 2005.) Second, there is considerable evidence that
catastrophic misinterpretations are not sufficient in themselves to produce panic. Rapee
(1995a) has argued that perceived uncontrollability is an important cognitive variable in
panic symptoms and Casey et al. (2004) have proposed an integrated model in which the
ongoing occurrence of panic is influenced by catastrophic misinterpretations of bodily
sensations and panic self- efficacy (i.e., positive cognitions that emphasize control or
coping). We would argue that a more comprehensive cognitive model of panic is needed
(see Figure 8.1) in which the extent of dissociation between an automatic catastrophic
misinterpretation and a more realistic, benign interpretation of bodily sensations will
determine the occurrence of panic attacks (Beck, 1988). In other words, the persistence
of panic symptoms may not only depend on the occurrence of catastrophic misinterpre-
tations but also on the inability to self- correct with a more realistic explanation of the
physical changes at the elaborative stage.
Two other criticisms of the catastrophic misinterpretation model must be men-
tioned. Defining what is meant by “catastrophe” has proven difficult. If a narrow defi-
nition is adopted in which catastrophe means an “imminent physical or psychological
harm” (e.g., heart attack, fainting, suffocation), than these types of interpretations are
relatively infrequent in panic disorder. Instead the most common threat interpretations
associated with physical symptoms is “fear of losing control” or “fear of an impending
panic attack,” or even some social threat such as being embarrassed in front of others
(Austin & Richards, 2001). Austin and Richards suggest that a much broader range of
outcomes should be included as “catastrophes.” Finally, more research is needed on the
causal links between body sensations, catastrophic cognitions, and panic symptoms.
Rachman (2004) has argued that it is difficult to determine if catastrophic cognitions
are the cause, the consequence, or merely a correlate of panic, although the biological
challenge experiments have been most informative in this regard.
Hypothesis 4. Interoceptive Amplification
The production of a catastrophic misinterpretation of internal cues will heighten the
intensity of the feared sensations in panic but not in nonpanic states.
According to the cognitive model, a positive feedback loop occurs with the auto-
matic catastrophic misinterpretation of bodily sensations directly contributing to a fur-
ther intensification of the physical or mental changes that were the initial source of
threat schema activation. An escalation in the feared sensations will fuel continued
activation of the physiological threat schemas, ensuring that the individual with panic
disorder becomes fixated on the catastrophic misinterpretation (Beck, 1988).
Few studies have directly investigated this hypothesis. Evidence of a moderate posi-
tive correlation between catastrophic cognitions and their corresponding bodily sensa-
tion (i.e., breathless-fear of suffocation) is consistent with the interoceptive amplifica-
tion hypothesis (e.g., Rachman et al., 1987; Street et al., 1989). D. M. Clark et al. (1988)
commented on a study conducted in their laboratory in which panic patients but not