Maximilian J Geiger1, Katharina Domschke1, Jonathan Ipser2, Coenie Hattingh2, David S Baldwin2,3, Christine Lochner4, Dan J Stein2,5. 1. a Department of Psychiatry , University of Wuerzburg , Wuerzburg , Germany. 2. b Department of Psychiatry and Mental Health , University of Cape Town , Cape Town , South Africa. 3. c Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton , Southampton , UK. 4. d MRC Unit on Anxiety and Stress Disorders, Department of Psychiatry , University of Stellenbosch , Stellenbosch , South Africa. 5. e Groote Schuur Hospital, MRC Unit on Anxiety and Stress Disorders, University of Cape Town , Cape Town , South Africa.
Abstract
OBJECTIVES: Research into the neural basis of social anxiety disorder (SAD) suggests alterations in prefrontal networks, which may in turn disrupt regulation of the limbic system. Better understanding of the disturbed interface between these networks may improve current pathogenic models of this disorder. METHODS: Applying group independent component analysis (ICA) to recordings of fMRI resting-state, connectivity in the executive control network was studied in 18 patients with SAD and 15 age- and sex-matched healthy controls. RESULTS: Results revealed a dissociation within the left executive control network, with SAD patients showing decreased connectivity of the orbitofrontal gyrus and increased connectivity of the middle frontal gyrus compared to healthy controls. In a subsequent seed-based functional connectivity analysis, patients with SAD displayed increased connectivity between the left orbitofrontal gyrus and the left amygdala. CONCLUSIONS: Findings suggest that hypo-connectivity in the executive control network and hyper-connectivity between the orbitofrontal cortex and the amygdala may reflect a disturbance in the balance between top-down and bottom-up control processes, potentially contributing to the development of SAD.
OBJECTIVES: Research into the neural basis of social anxiety disorder (SAD) suggests alterations in prefrontal networks, which may in turn disrupt regulation of the limbic system. Better understanding of the disturbed interface between these networks may improve current pathogenic models of this disorder. METHODS: Applying group independent component analysis (ICA) to recordings of fMRI resting-state, connectivity in the executive control network was studied in 18 patients with SAD and 15 age- and sex-matched healthy controls. RESULTS: Results revealed a dissociation within the left executive control network, with SADpatients showing decreased connectivity of the orbitofrontal gyrus and increased connectivity of the middle frontal gyrus compared to healthy controls. In a subsequent seed-based functional connectivity analysis, patients with SAD displayed increased connectivity between the left orbitofrontal gyrus and the left amygdala. CONCLUSIONS: Findings suggest that hypo-connectivity in the executive control network and hyper-connectivity between the orbitofrontal cortex and the amygdala may reflect a disturbance in the balance between top-down and bottom-up control processes, potentially contributing to the development of SAD.
Entities:
Keywords:
amygdala; attention; fMRI; prefrontal cortex; social phobia
Authors: Janna Marie Bas-Hoogendam; Henk van Steenbergen; J Nienke Pannekoek; Jean-Paul Fouche; Christine Lochner; Coenraad J Hattingh; Henk R Cremers; Tomas Furmark; Kristoffer N T Månsson; Andreas Frick; Jonas Engman; Carl-Johan Boraxbekk; Per Carlbring; Gerhard Andersson; Mats Fredrikson; Thomas Straube; Jutta Peterburs; Heide Klumpp; K Luan Phan; Karin Roelofs; Dick J Veltman; Marie-José van Tol; Dan J Stein; Nic J A van der Wee Journal: Neuroimage Clin Date: 2017-08-30 Impact factor: 4.881