Anxiety Disorders Clinical Trial
Official title:
Generalized Anxiety Disorder and Social Anxiety Disorder: Their Impact on the Processing of Social Emotional Information and Instrumental Learning
The purpose of this study is to increase researchers understanding of the biological basis of
generalized anxiety disorder and social anxiety disorder. They will investigate how the brain
activity associated with specific thoughts and feelings may play a role in these anxiety
disorders. This knowledge will be used to design interventions to help those with these
illnesses.
To qualify for this study, participants must be evaluated via an initial telephone screening
interview and material sent through the mail.
Participants will then be required to make three visits to NIH. During the first visit, they
will be asked questions about their general mood, degree of nervousness, thinking skills, and
behavior. They will undergo a thorough physical exam, including an EKG, blood work,
urinalysis, and a pregnancy test for women of childbearing potential. During the second
visit, participants will spend about 2.5 hours doing various tasks while sitting and looking
at a computer screen. These tasks will guide them to experience specific kinds of thoughts
and emotions. Researchers will attach electrodes to the participants hands to monitor the
amount of electricity conducted by the skin. The third visit will be similar to the second
visit, but participants will perform the tasks while lying in a MRI scanner.
Participants will be compensated up to $400 for their involvement in this study.
There have been suggestions that the threshold for amygdala activity is lower in individuals
with anxiety disorders than in healthy individuals. However, despite it's immediate
plausibility, there have been relatively few tests of this hypothesis. Specifically, there
have been very few explorations of the performance of patients with anxiety disorders on
measures known to implicate the amygdala.
Although the high co-morbidity of Generalized Anxiety Disorder (GAD) and Social Anxiety
Disorder (SAD) complicates the issue, the fact that the disorders doubly dissociate suggests
that they are due to dysfunctional activity in separable neurocognitive systems. We would
suggest that the hyper-responsive amygdala hypothesis is more likely to be linked to the
explanation of GAD. In contrast, SAD may be due to reduced activation thresholds for units in
a system that responds to social threat and which recruits lateral orbital frontal cortex.
Thus, the current project will determine the performance of patients with GAD and SAD on
measures in which the amygdala is known to play a role and also measures that recruit lateral
orbital frontal cortex and the system for social response reversal. In addition, two proposed
neuro-imaging studies will directly assess neural responses in these two systems in both
patient populations. The project should provide clear data that will constrain future
theorizing on the pathology implicated in these two disorders.
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