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Mechanisms of Virtual Reality Exposure Therapy: The Role of the Behavioral Activation and Behavioral Inhibition Systems

Wilhelm, Frank ; Pfaltz, Monique ; Gross, James ; Mauss, Iris ; Kim, Sun ; Wiederhold, Brenda

In: Applied Psychophysiology and Biofeedback, 2005, vol. 30, no. 3, p. 271-284

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    Title
    • Mechanisms of Virtual Reality Exposure Therapy: The Role of the Behavioral Activation and Behavioral Inhibition Systems
    Author
    • Wilhelm, Frank. Institute for Psychology, University of Basel, Basel, Switzerland
    • Pfaltz, Monique. Institute for Psychology, University of Basel, Basel, Switzerland
    • Gross, James. Department of Psychology, Stanford University, Stanford, California
    • Mauss, Iris. Department of Psychology, Stanford University, Stanford, California
    • Kim, Sun. Department of Biomedical Engineering, College of Medicine, Hanyang University, Seoul, Korea
    • Wiederhold, Brenda. Virtual Reality Medical Center, Interactive Media Institute, San Diego, California
    Document Type
    • Postprint
    Language
    • English
    Published in
    • Applied Psychophysiology and Biofeedback, 2005, vol. 30, no. 3, p. 271-284. Kluwer Academic Publishers-Plenum Publishers
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:310033
    Summary
    J. A. Gray's (1975) theory distinguishes between two motivational systems, which he refers to as the behavioral activation system (BAS) and the behavioral inhibition system (BIS). D. C. Fowles (1980) has shown that heart rate responses reflect activity of the BAS, and electrodermal responses reflect activity of the BIS. Both BAS and BIS are reliably activated during in-vivo exposure to fearful situations (F. H. Wilhelm & W. T. Roth, 1998). However, due to the constraints imposed by virtual reality (VR), we hypothesized that VR exposure to fearful situations would activate the BIS alone. To test this hypothesis, a VR free-standing elevator simulation was presented to participants selected for high and low fear of heights. As predicted, the high-anxious group strongly responded electrodermally (effect size d = 1.53), but showed only minimal HR elevations during exposure (d = 0.12), and little other cardiovascular or respiratory changes. The low-anxious control group showed little electrodermal and HR reactivity (d = 0.28 and 0.12). A comparison with data from a previous study demonstrated that this pattern was in stark contrast to the large electrodermal and cardiovascular response observed during situational in-vivo exposure outside the laboratory. We conclude that the BIS, but not BAS, is selectively activated during VR exposure, causing discordance between self-report and commonly used physiological measures of anxiety. Results are discussed within the framework of E. B. Foa & M. J. Kozak's (1986) emotional processing theory of fear modification, suggesting different mechanisms underlying VR and in-vivo exposure treatments