Panic Disorder 289
Cognitive theory of paniC DisorDerDescription of the Model
Panic attacks are an immediate fear response and so the psychogenic processes primar-
ily responsible for the onset and persistence of panic occur within Phase I of the cogni-
tive model depicted in Chapter 2 (see Figure 2.1). The key cognitive processes of panic,
then, occur at an automatic level of activation. The Phase II processes, representing
deliberate, elaborative efforts to cope with heightened anxiety and the anticipation of
panic, are secondary contributors to the persistence of the disorder. In this way the cog-
nitive basis of panic is entirely different from that of GAD where Phase II processes play
a more critical role in the disorder. The cognitive model of panic was first articulated in
the mid- to late 1980s by Beck and colleagues (Beck, 1988; Beck et al., 1985; Beck &
Greenberg, 1988; D. M. Clark & Beck, 1988) and further elaborated by D. M. Clark
(1986a, 1988, 1996; D. M. Clark et al., 1988). Derived from these earlier accounts,
Figure 8.1 illustrates the current cognitive explanation for panic based on the generic
cognitive model (i.e., Figure 2.1). It should be noted that the cognitive model was formu-
lated to explain the pathogenesis of recurrent panic attacks or panic disorder. It has less
relevance for understanding the occasional panic attacks found in the general popula-
tion or the occurrence of nonfearful panic-like somatic symptoms prominent in medical
settings (D. M. Clark, 1997; see also Eifert, Zvolensky, & Lejuez, 2000).
Activation and Attention
Changes in internal states such as the occurrence or intensification of certain physical
sensations (e.g., chest tightness, breathlessness, increased heart rate, nauseous feelings)
or mental processes (e.g., mind goes blank, sense of derealization) are the primary
triggers for panic attacks. In most cases of recurrent panic external stimuli or situ-
ations will become triggers, but only because they have the capacity to elicit bodily
sensations that are perceived as threatening (D. M. Clark, 1986a). In our case example
Helen’s primary trigger for panic was a sense of breathlessness. However, she perceived
changes in her breathing whenever she was in novel situations and so unfamiliar set-
tings such as travel outside her community, visiting new people, and so on began to
trigger heightened anxiety and anticipated panic. Naturally she started avoiding these
situations because they elicited the threatening somatic sensation, breathlessness. In
severe agoraphobia a wide variety of external situations can trigger panic but only
because they elicit some feared internal state. The physical and mental processes that
are misperceived as an imminent threat are most often due to anxiety, and less often
due to other emotional states, stress, physical exertion, ingestion of substances with
caffeine or other chemicals, or even the natural ebb and flow of physiological function
(D. M. Clark, 1986a, 1988, 1996).
As noted in Figure 8.1, individuals prone to panic are oriented toward selectively
attending to internal somatic or mental processes. They are hypervigilant for the expe-
rience of these sensations and focus their attention on any change in functioning that
might seem abnormal (Beck, 1988). The orienting mode in panic disorder is primed
toward rapid detection of interoceptive cues that could represent an immediate and
imminent danger to survival. This early detection process is automatic and noncon-
scious, resulting in a hypersensitivity to bodily sensations.