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VENTROMEDIAL PREFRONTAL CORTEX REACTIVITY IS ALTERED IN GENERALIZED ANXIETY DISORDER DURING FEAR GENERALIZATION

Authors

  • Tsafrir Greenberg M.A.,

    1. Department of Psychology, State University of New York at Stony Brook, New York
    2. Department of Biomedical Engineering, State University of New York at Stony Brook, New York
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  • Joshua M. Carlson Ph.D.,

    1. Department of Biomedical Engineering, State University of New York at Stony Brook, New York
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  • Jiook Cha M.S.,

    1. Department of Biomedical Engineering, State University of New York at Stony Brook, New York
    2. Program in Neuroscience, Department of Neurobiology and Behavior, State University of New York at Stony Brook, New York
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  • Greg Hajcak Ph.D.,

    1. Department of Psychology, State University of New York at Stony Brook, New York
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  • Lilianne R. Mujica-Parodi Ph.D.

    Corresponding author
    1. Program in Neuroscience, Department of Neurobiology and Behavior, State University of New York at Stony Brook, New York
    • Department of Biomedical Engineering, State University of New York at Stony Brook, New York
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Correspondence to: Lilianne R. Mujica-Parodi, Laboratory for Computational Neurodiagnostics, Department of Biomedical Engineering, Bioengineering Building Room 119, State University of New York at Stony Brook, Stony Brook, NY 11794.

E-mail: lilianne.strey@stonybrook.edu

Abstract

Background

Fear generalization is thought to contribute to the development and maintenance of anxiety symptoms and accordingly has been the focus of recent research. Previously, we reported that in healthy individuals (N = 25) neural reactivity in the insula, anterior cingulate cortex (ACC), supplementary motor area (SMA), and caudate follow a generalization gradient with a peak response to a conditioned stimulus (CS) that declines with greater perceptual dissimilarity of generalization stimuli (GS) to the CS. In contrast, reactivity in the ventromedial prefrontal cortex (vmPFC), a region linked to fear inhibition, showed an opposite response pattern. The aim of the current study was to examine whether neural responses to fear generalization differ in generalized anxiety disorder (GAD). A second aim was to examine connectivity of primary regions engaged by the generalization task in the GAD group versus healthy group, using psychophysiological interaction analysis.

Methods

Thirty-two women diagnosed with GAD were scanned using the same generalization task as our healthy group.

Results

Individuals with GAD exhibited a less discriminant vmPFC response pattern suggestive of deficient recruitment of vmPFC during fear inhibition. Across participants, there was enhanced anterior insula (aINS) coupling with the posterior insula, ACC, SMA, and amygdala during presentation of the CS, consistent with a modulatory role for the aINS in the execution of fear responses.

Conclusions

These findings suggest that deficits in fear regulation, rather than in the excitatory response itself, are more critical to the pathophysiology of GAD in the context of fear generalization.

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