TopIntroduction
There is a growing body of research indicating the multiple ways that affective dysregulation (e.g., anxiety disorders, specific phobias, panic disorder, and post-traumatic stress disorder (PTSD)) may lead to significant impairments in normal life functioning. Anxiety and fear are concentrated emotional experiences that serve critical functions in organizing necessary survival responses (Fendt & Fanselow, 1999). In properly functioning affective systems, the responses are adaptive. LeDoux (2012a) posits survival circuits that enable humans to adapt to feared stimuli by organizing brain functions. The fear induced arousal and activation of survival circuits allows for adaptive responses to take priority and other responses are inhibited. Further, attentional processing focuses on pertinent environmental stimuli and learning occurs (Scherer, 2000; LeDoux, 2012b). Hence, adaptive survival circuits are optimized to detect threatening stimuli and relay the information as environmental challenges and opportunities. The adaptive survival circuits use this information to adjust behavioral and psychophysiological responses for appropriate adaptation and resolution. Excessive fear responses, however, can be restrictive and may be a sign of dysregulated anxiety. When exposure to stress occurs early in development and is repeated in persons with a particular genetic disposition, a decreased threshold for developing anxiety may result (Heim & Nemeroff, 1999). Further, over-excitation and deprivation can influence the affective system and may induce changes in the emotional circuitry of the brain that can contribute to stress-related psychopathology (Davidson, Jackson, & Kalin, 2000).
A good deal of research has shown that exposure therapy is effective for reducing negative affective symptoms (Rothbaum & Schwartz, 2002). In vivo exposure therapy has been found to have greater efficacy when compared to imaginal exposure, especially in the treatment of specific phobias (Emmelkamp, 2003). Exposure to emotional situations and prolonged rehearsal result in the regular activation of cerebral metabolism in brain areas associated with inhibition of maladaptive associative processes (Schwartz, 1998). Identical neural circuits have been found to be involved in affective regulation across affective disorders (De Raedt, 2006; Mineka, Watson, & Clark, 1998). Systematic and controlled therapeutic exposure to phobic stimuli may enhance emotional regulation through adjustments of inhibitory processes on the amygdala by the medial prefrontal cortex during exposure and structural changes in the hippocampus after successful therapy (Hariri, Bookheimer, & Mazziotta, 2000).
A novel tool for conducting exposure therapy is virtual reality exposure therapy (VRET), in which users are immersed within a computer-generated simulation or virtual environment (VE) that updates in a natural way to the user’s psychophysiological arousal, head and/or body motion (Parsons and Courtney, 2011, Parsons and Reinebold, 2012). Virtual environment applications that focus on treatment of affective (see Powers & Emmelkamp, 2008; Parsons et al., 2008a; Opris et al., 2012) and cognitive disorders (see Rose et al., 2005; Parsons 2009a) as well as assessment of component cognitive processes are now being developed and tested: attention (Parsons, et al., 2007, 2011) spatial abilities (Beck et al., 2010; Goodrich-Hunsaker and Hopkins, 2010; Parsons, et al., 2013), memory (Moffat, 2009; Parsons & Rizzo, 2008b; Parsons et al., 2013; Knight & Titov, 2009), spatial memory (Parsons et al., 2013); and executive functions (Armstrong et al., 2013; Henry et al., 2012; Parsons et al., 2012, 2013, 2014). The increased ecological validity of virtual scenarios may aid differential diagnosis and treatment planning. Within a virtual world, it is possible to systematically present cognitive tasks targeting neuropsychological performance beyond what are currently available using traditional methods (Parsons, 2011, 2012).