Highlighting Faculty Member Michelle Craske
Date published: 8/1/2018
My lab investigates the cognitive, behavioral and biological risk factors and correlates of anxiety and depression in order to develop novel treatments. We take a multidisciplinary, science-driven approach and have a commitment to bringing our findings into clinical practice settings.
We’ve observed that anxious or depressed individuals tend to pay more attention to threat-relevant stimuli, and interpret ambiguous information as being threatening. These individuals also react more strongly to cues that signal threat, and respond more weakly to 1) cues that signal safety in threatening situations, and 2) signals that previously signaled threat, but no longer signal threat. Because of these findings, we are beginning to evaluate overgeneralization of fear learning following aversive experiences as another risk factor for anxiety and depression. We have hypothesized that it is very likely that the combination of these factors contribute to the onset of pervasive and persistent anxiety or depression.
Fear generalization is a defining feature of anxiety disorders. Essentially, fear generalization is when a person ‘learns’ a fear response towards a stimulus, and then generalizes the response to other stimuli that are related to the original feared stimulus. We have argued that fear generalization following trauma can be reduced through the administration of glucose. Extending the work of animal scientists, we have shown that the administration of glucose increased context fear conditioning (learning to predict aversive events), which could lead to decreased fear generalization.
I have studied mechanisms of exposure therapy for many years, mostly by translating from the science of fear conditioning and extinction, and more recently the neuroscience of linguistic processing. We have studied several methods for enhancing inhibitory associations during exposure therapy and their retrieval once the therapy is over, and have had success with “deepened extinction” and “occasional reinforced extinction” within laboratory settings and in samples of individuals who have phobias.
We have also explored ways of increasing the positive valence (positive feelings) associated with a conditioned stimulus. Further, we have demonstrated context renewal, a resurgence of fear when tested in a context that differs from the extinction/exposure context, as a pathway through which fear returns following exposure therapy. Extending from animal science, we have investigated ways to decrease the context specificity of extinction learning and thus reduce return of fear following exposure therapy.
Another method of enhancing inhibitory regulation during exposure therapy involves linguistic processing. Our findings suggest that labeling of affect (emotion), as opposed to more traditional cognitive therapy which attempts to change the content of appraisals, may improve inhibitory regulation during exposure. We have demonstrated benefits of affect labeling during exposure for phobias and posttraumatic stress.
My treatment research has extended to bringing Cognitive Behavioral Therapy (CBT) into the real world setting of primary care, where there are many anxious and depressed patients present. We developed a comprehensive computer assisted CBT program, that guides not only the patient but also the novice clinician, and thereby maintains fidelity of CBT in real world settings. With current funding, we are now investigating a similar model of treatment delivery (using an internet platform to guide novice clinicians and patients) for cognitive behavioral therapy for social anxiety disorder among the people who are unemployed.