Exposure is an important, if not the most important, treatment component of effective interventions for the range of anxiety disorders, including social phobia (e.g., Feske & Chambless, 1995
), panic disorder and agoraphobia (e.g., Clum, Clum, & Surls, 1993
), obsessive-compulsive disorder (e.g., Abramowitz, 1997
), post-traumatic stress disorder (e.g., Foa et al., 1999
), and specific phobias (e.g., Öst, Svensson, Hellstrom, & Lindwall, 2001
). A case in point is social phobia. The prominent model of social phobia is the cognitive perspective, which assumes that effective psychological treatment needs to change the person’s self-perception in a more positive direction (Clark & Wells, 1995
). Therefore, some investigators argued that a treatment that specifically targets dysfunctional beliefs about social situations should be more effective than simple exposure procedures. The literature reports eight controlled clinical studies in which investigators directly compared cognitive-behavioral therapy to exposure therapy without explicit cognitive interventions (Butler, Cullington, Munby, Amies, & Gelder., 1984
; Emmelkamp, Mersch, Vissia, van der Helm, 1985
; Gelernter et al., 1991
; Hofmann, 2004
; Hope, Herbert, & White, 1995
; Mattick & Peters, 1988
; Mattick, Peters, & Clark, 1989
; Scholing & Emmelkamp, 1993a,b). In only two of the trials did the effects of cognitive-behavior therapy exceed those of exposure alone at post-treatment (Butler et al., 1984
; Mattick & Peters, 1988
). These component analyses studies were based on the assumption that simple exposure procedures are sub-optimal because the mechanism of change is via extinction learning, which is not mediated by cognitive changes. However, based on the present review, there is no evidence to support this assumption. Instead, the empirical evidence suggests that exposure procedures without explicit cognitive intervention strategies have very similar effects than comprehensive cognitive-behavioral treatments, simply because exposure therapy is mediated through changes in cognitions, and specifically changes in CS-US (harm) expectancy.
The efficacy of exposure therapy as compared to other, more comprehensive, treatment approaches has been surprising to many researchers. Moreover, it has been surprising that exposure therapy not only alleviates specific anxiety symptoms but is also associated with improvement in general functioning and results in significant cognitive changes. For example, after reviewing the outcome literature of CBT and exposure therapy without explicit cognitive intervention for social phobia, Feske and Chambless (1995)
“Overall, CBT and exposure yielded very similar pre-post and prefollow-up effect for self-report measures of social phobia, cognitive symptoms, and depressed/anxious mood. Moreover, there was no evidence of differential dropout between the two treatment modalities. These findings are disappointing in light of the enthusiasm for CBT. In particular, investigators had hoped that CBT would lead to greater improvement in cognitive distortions associated with social phobia and would thus produce more generalized and durable treatment effects than exposure without explicit cognitive components” (pp. 712-713).
These findings are only surprising if we assume that exposure therapy (and extinction) only involves primitive, automatic, and low-level processes that need to be supplemented with cognitive therapy to effectively target dysfunctional cognitive processes. If, on the other hand, we assume that exposure therapy is cognitively mediated, we would expect exposure therapy to have very similar effects as more comprehensive treatments, such as cognitive therapy. In fact, my research group has found that repeated exposures to feared public speaking situations lead to very similar short-term reductions of social anxiety symptoms than a comprehensive cognitive-behavioral treatment that targets a variety of dysfunctional thoughts related to social phobia (Hofmann, Moscovitch, Kim, & Taylor, 2004
). Moreover, it has been shown that treatment changes during cognitive-behavioral therapy and exposure therapy are both mediated via changes in cognitions (Hofmann, 2004
). These results are consistent with previous studies suggesting that simple exposure procedures lead to significant improvements in negative self-perception (Hofmann, 2000
) and other negative cognitions (Newman, Hofmann, Trabert, Roth, & Taylor, 1994
). These data illustrate the importance of cognitive processes in exposure therapy. Although the precise mechanism of treatment change during exposure therapy remains unclear, it can be concluded that repeated exposure practices (whether with or without explicit cognitive strategies) change harm expectancy, among other things. The effect of exposure therapy on other cognitive variables, such as changes in negative self-perception in social phobia, is difficult to explain at this stage and will require additional research.
Recognizing the importance of cognitive processes in fear acquisition, extinction, and exposure therapy offers a new possibility for intervention research, namely to improve the effects of exposure therapy with pharmacological interventions that are believed to act as cognitive enhancers. Animal research has shown that fear and extinction learning are both blocked by antagonists at the glutamatergic N
-methyl-d-aspartate (NMDA) receptor, which is critically involved in learning and memory. For example, intra-amygdala infusions of an NMDA receptor antagonist shortly before extinction training dose-dependently block extinction (Falls, Miserendino, & Davis, 1992
). Moreover, d-cycloserine (DCS), a partial NMDA agonist dose-dependently enhances extinction in rats (Ledgerwood, Richardson, Cranney, 2003
; Walker, Ressler, Lu, & Davis, 2002
). Interestingly, DCS can still facilitate extinction when given up to about 3 h after extinction training, which suggests that DCS acts to facilitate memory consolidation of extinction (Richardson, Ledgerwood, & Cranney, 2004
In an initial effort to demonstrate the utility of DCS as a method to enhance exposure therapy in humans, Ressler et al. (2004)
randomized 28 subjects with a DSM-IV diagnosis (APA, 1994
) of specific phobia of heights (acrophobia) to 2 sessions of virtual reality exposure therapy preceded in double-blind fashion by administration of single doses of placebo or DCS (50 or 500 mg) taken 2-4 h prior to each of the sessions. Exposure therapy combined with DCS resulted in significantly larger reductions of acrophobia symptoms at 1 week and 3 months following treatment with no difference in efficacy between the 2 doses and no reports of adverse effects from DCS administration. Subjects receiving DCS also showed significantly greater decreases in post-treatment skin conductance fluctuations during the virtual exposure and significantly greater improvement compared to placebo on general measures of real-world acrophobia symptoms that were evident early in treatment and were maintained at 3 months.
In another double-blind placebo-controlled study, 27 patients with a principal DSM-IV diagnosis of social anxiety disorder (social phobia) were assigned to either receive 5 exposure group sessions plus DCS (50 mg) or 5 exposure group sessions plus pill placebo (Hofmann et al., 2006
). The exposure practices of increasing difficulty consisted of giving speeches about topics, chosen by the therapists, in front of the other group members or confederates and a video camera. The level of social anxiety was assessed at baseline, post-treatment, and 1 month after the last session (1-month follow-up). The results showed that patients who received DCS prior to the exposure sessions showed greater reduction in their social anxiety than patients who received placebo prior to the exposures. The difference between the two groups increased linearly with time, with the greatest treatment effects of DCS being evident at follow-up.
Together, the clinical outcome studies by Hofmann et al. (2006)
and Ressler et al. (2004)
provide support for the use of a cognitive enhancer to augment exposure therapy in patients with anxiety disorders. However, the evidence is still preliminary and a number of additional studies around the world are currently being conducted to replicate and extend these early findings and to dissect the specific mechanism.