302 TREATMENT OF SPECIFIC ANXIETY DISORDERS
would be a pleasant or benign experience. Findings from these studies indicate that type
of information provided, expectations, perceived control, and presence of safety cues
influence individuals’ anxiety and arousal to the induction (Khawaja & Oei, 1998). For
example, in a study of healthy individuals who received sodium lactate and a placebo
on two different days, only those who received the lactate infusion and anxious instruc-
tions experienced a significant increase in anxiety (van der Molen, van den Hout, Vroe-
men, Lousberg, & Griez, 1986).
Over the years numerous studies have demonstrated that individuals with panic
disorder show greater reactivity to inhaled carbon dioxide (CO 2 ) than other anxiety
disorder groups and healthy controls by experiencing more intense bodily sensations,
and greater likelihood of panic symptoms and elevated anxiety as indicated by sub-
jective measures, even though there are few differences in physiological functioning
(e.g., Perna, Barbini, Cocchi, Bertani, & Gasperini, 1995; Perna et al., 2004; Rapee et
al., 1992; Verburg, Griez, Meijer, & Pols, 1995). Furthermore, individuals with panic
disorder report that the symptoms produced by CO 2 inhalation are similar to real-life
panic attacks (Fyer et al., 1987; van den Hout & Griez, 1984; see review by Rapee,
1995a). It appears that affective response to CO 2 inhalation may even have etiological
significance. In a 2-year follow-up study, Schmidt, Maner, and Zvolensky (2007) found
that CO 2 reactivity predicted the later development of panic attacks. However, there are
individual differences even among panic disorder individuals in their response to CO 2
inhalation, with 55–80% reporting a panic attack (Perna et al., 1995, 2004; Rapee et
al., 1992). Rapee (1995a) noted that individuals who respond to a biological challenge
are more likely to experience symptoms that are similar to their real-life panic symp-
toms and to report thoughts of impending catastrophe. He concluded that individuals
will exhibit a greater affective response to biological challenges if they associate an
immediate impending physical or mental catastrophe (threat) with the induced sensa-
tions and perceive diminished control over the aversive experience (e.g., Rapee et al.,
1992; Sanderson, Rapee, & Barlow, 1989). Consistent with this conclusion Rapee et al.
(1992) found that the only significant predictor of fear associated with hyperventilation
and CO 2 inhalation was ASI Total Score (see also Rassovsky et al., 2000). Overall these
findings are entirely consistent with the catastrophic misinterpretation hypothesis.
Additional support for the hypothesis is evident in recent studies that investigated
information processing of physical stimuli and induction of physical symptoms. Using a
modified semantic priming experiment, Schneider and Schulte (2007) found that indi-
viduals with panic disorder exhibited a significantly higher automatic (but not strategic)
priming effect for idiographically selected anxiety symptom primes followed by cata-
strophic interpretations than nonclinical controls. The authors interpret this automatic
priming effect as a consequence of strong idiographic associations produced by the rela-
tion of catastrophic thoughts to bodily symptoms during panic attacks. More specifi-
cally, there is evidence that imposing a respiratory load influences processing bias for
negative physical words in those with fear of suffocation (Kroeze et al., 2005; see also
Nay, Thorpe, Robertson-Nay, Hecker, & Sigmon, 2004).
In summary there is strong empirical support for the catastrophic misinterpretation
hypothesis (see Austin & Richards, 2001; Khawaja & Oei, 1998; Casey et al., 2004;
Rapee, 1995a). Misinterpreting physical or mental sensations as signifying an imminent
threat has been consistently found in self- report, clinical, and experimental studies and
its presence influences the intensity of panic symptoms. However, there are a number of