期刊
MOLECULAR PSYCHIATRY
卷 27, 期 1, 页码 164-179出版社
SPRINGERNATURE
DOI: 10.1038/s41380-021-01154-6
关键词
-
资金
- Australian Government Research Training Program Scholarship
The review synthesized findings from 35 studies on resting-state brain alterations in social anxiety disorder, showing both higher and lower connectivity in different brain regions, particularly between frontal-amygdala and frontal-parietal regions in individuals with social anxiety disorder. The frontal regions were consistently implicated across studies and most associated with social anxiety symptoms, suggesting potential neurobiological targets for treatment.
There has been a growing interest in resting-state brain alterations in people with social anxiety disorder. However, the evidence has been mixed and contested and further understanding of the neurobiology of this disorder may aid in informing methods to increase diagnostic accuracy and treatment targets. With this systematic review, we aimed to synthesize the findings of the neuroimaging literature on resting-state functional activity and connectivity in social anxiety disorder, and to summarize associations between brain and social anxiety symptoms to further characterize the neurobiology of the disorder. We systematically searched seven databases for empirical research studies. Thirty-five studies met the inclusion criteria, with a total of 1611 participants (795 people with social anxiety disorder and 816 controls). Studies involving resting-state seed-based functional connectivity analyses were the most common. Individuals with social anxiety disorder (vs. controls) displayed both higher and lower connectivity between frontal-amygdala and frontal-parietal regions. Frontal regions were the most consistently implicated across other analysis methods, and most associated with social anxiety symptoms. Small sample sizes and variation in the types of analyses used across studies may have contributed to the inconsistencies in the findings of this review. This review provides novel insights into established neurobiological models of social anxiety disorder and provides an update on what is known about the neurobiology of this disorder in the absence of any overt tasks (i.e., resting state). The knowledge gained from this body of research enabled us to also provide recommendations for a more standardized imaging pre-processing approach to examine resting-state brain activity and connectivity that could help advance knowledge in this field. We believe this is warranted to take the next step toward clinical translation in social anxiety disorder that may lead to better treatment outcomes by informing the identification of neurobiological targets for treatment.
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