Our analyses of the premises of EPT failed to produce compelling results to support the veracity of that theory. Neither IFA nor WSH during exposure had any relationship to outcomes. The lack of evidence for level of activation predicting treatment outcome may be due to the most fearful participants refusing to participate in the study, as well as designing exposure tasks that maximized IFA for all participants. These two factors limit the range of relationship within the sample and renders a complete analysis of the efficacy of activation in treatment of acrophobia impossible. The same, however, cannot be said of the other two factors of emotional processing theory. The lack of evidence for WSH is astounding, as none of the 8 analyses aimed at uncovering the efficacy of this process yielded significant results. Beyond that, the amount of unique variance that is explained by WSH was miniscule (ranging from 0 to 4.7%).
Some support was found for the role of BSH for predicting change from baseline to immediate, but the effects were restricted to the same response domain of measurement, such that reported anxiety predicted changes in reported anxiety and heart rate predicted changes in heart rate. Furthermore, for the most part, these effects did not extend to baseline to post outcomes. This inconsistent finding on BSH may be due to the fact that its measurement was confounded with the outcome measure due to the proximity in measurement schedule. In addition, no relationship was found between WSH and BSH. This is especially problematic for EPT, as WSH is presumed to be a necessary prerequisite for BSH.
These results raise serious doubts about the role of within-session habituation as a mechanism of change, and while between-session habituation may have some limited effects immediately, there appear to be other more important factors that play into long-term results of exposure therapy.
While this study failed to produce results that supported the hypotheses behind EPT as a moderator of improvement in exposure, this study is telling about the viability of the theory. EPT has found scant support over the twenty-plus years in existence (see Craske et al., 2008
for review), and this study was unable to produce any results that support the over-arching theory. This would seem to suggest that EPT is not a viable explanation of the mechanism of change in exposure therapy, and further research should look to uncover possible alternative theories to explain this phenomenon.
An alternative to EPT could come from advances in the basic science of fear learning (Craske et al., 2008
). Expectancies regarding the likelihood of aversive events are central to human fear conditioning. For example, contingency awareness (i.e., knowledge that a specific CS predicts a US), although of debatable necessity
for conditioned responding (e.g., Lovibond & Shanks, 2002
, versus Ohman & Mineka, 2001
) is a strong correlate of conditioned responding. Differential autonomic conditioning in particular is strongly associated with verbal measures of contingency knowledge (e.g., Purkis & Lipp, 2001
). Expectancies also are important for extinction; extinction is posited to follow from a mismatch between the expectancy of an aversive event and the absence of its occurrence (Rescorla & Wagner, 1972
), or from the perception of a negative change in the rate at which aversive events are associated with the CS (Gallistel & Gibbon, 2000
). Future research should build upon the wealth of research in animal models for fear conditioning in extinction in order to better understand the mechanisms of change in exposure base treatments.
One example of how this could be done is by looking to the animal research on temporal expectancies. The duration for which exposure to the CS continues may be critical in the process of extinction, since durations that exceed the temporal expectancy for the US may serve as potent mismatches. Rodent research with mice indicates that extinction is more effective when individual CS presentations are massed, and blocks of massed CSs are spaced apart (Cain, Blounin, & Barad, 2003
). These data have been interpreted to suggest that durations of a continuous CS presentation during extinction that exceed the length of the CS during acquisition induces extinction learning most effectively by violating the temporal expectancy of the US, and that once induced, extinction learning is best consolidated with spaced training. Thus disconfirmation of temporal expectancy may be a means for enhancing learning through exposure therapy and should be fully explored to this end.
Another alternative would be to further explore potential cognitive mechanisms that may underlie the effectiveness of exposure based treatments. From one perspective the above potential mechanism of mismatches in expectancies is akin to cognitive models. The above the explanation merely works with the model in a way that does not demand that the cognitive processing needs to be explicit. That being said, more exploration in needed to uncover whether cognitive awareness has any mediating or moderating effects on the effectiveness of exposure based treatments.