Neuroimaging in social anxiety disorder: a systematic review of the literature
Open accessAbstract
Brain imaging techniques allow the in vivo evaluation of the human brain, leading to a better understanding of its anatomical, functional and metabolic substrate. The aim of this current report is to present a systematic and critical review of neuroimaging findings in Social Anxiety Disorder (SAD). A literature review was performed in the PubMed Medline, Scielo and Web of Science databases using the following keywords: 'MRI', 'functional', 'tomography', 'PET', 'SPECT', 'spectroscopy', 'relaxometry', 'tractography' and 'voxel' crossed one by one with the terms 'social anxiety' and 'social phobic', with no limit of time. We selected 196 articles and 48 of them were included in our review. Most of the included studies have explored the neural response to facial expressions of emotion, symptoms provocation paradigms, and disorder-related abnormalities in dopamine or serotonin neurotransmission. The most coherent finding among the brain imaging techniques reflects increased activity in limbic and paralimbic regions in SAD. The predominance of evidence implicating the amygdala strengthens the notion that it plays a crucial role in the pathophysiology of SAD. The observation of alterations in pre-frontal regions and the reduced activity observed in striatal and parietal areas show that much remains to be investigated within the complexity of SAD. Interesting, follow-up designed studies observed a decrease in perfusion in these same areas after either by pharmacological or psychological treatment. The medial prefrontal cortex provided additional support for a corticolimbic model of SAD pathophysiology, being a promising area to investigation. Furthermore, the dopaminergic and GABAergic hypotheses seem directed related to its physiopathology. The present review indicates that neuroimaging has contributed to a better understanding of the neurobiology of SAD. Although there were several methodological differences among the studies, the global results have often been consistent, reinforcing the evidence of a specific cerebral circuit involved in SAD, formed by limbic and cortical areas.
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Relative to healthy controls, people with SAD show atypical activity and connectivity between the amygdala and prefrontal regions.
“Compared to healthy individuals, individuals with SAD demonstrate aberrant activity in and connectivity between the amygdala and prefrontal regions (Freitas-Ferrari et al., 2010).”
From Changes in functional connectivity with cognitive behavioral therapy for social anxiety disorder predict outcomes at follow-up (2020) · cites this paper as Freitas-Ferrari et al., 2010
The fMRI section reports greater amygdala activation in people with SAD than in healthy controls and notes alterations in prefrontal regions. The Discussion describes impaired amygdala–prefrontal communication as a possible feature of anxiety disorders generally, but does not establish altered connectivity between those regions in SAD relative to healthy controls. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredNumerous studies have found greater amygdala activity in SAD compared to healthy controls in response to socially threatening stimuli.
“Numerous studies have found greater amygdala activity in SAD compared to healthy controls in response to socially threatening stimuli (see Brühl et al., 2014; Etkin & Wager, 2007; and Freitas-Ferrari et al., 2010 for reviews and meta-analyses)”
From Neural responses to social threat and predictors of cognitive behavioral therapy and acceptance and commitment therapy in social anxiety disorder (2017) · cites this paper as Freitas-Ferrari et al., 2010
The lack of neural hyperactivity in SAD and overall lack of significant group differences observed here conflicts with previous work comparing SAD individuals with healthy controls.
“The lack of neural hyperactivity in SAD and overall lack of significant group differences observed here conflicts with previous work comparing SAD individuals with healthy controls (Brühl et al., 2014; Freitas-Ferrari et al., 2010).”
From Neural responses to social threat and predictors of cognitive behavioral therapy and acceptance and commitment therapy in social anxiety disorder (2017) · cites this paper as Freitas-Ferrari et al., 2010
The dominant neurobiological model of anxiety disorders proposes that amygdala hyperreactivity corresponds to heightened emotional reactivity, while disrupted prefrontal processing corresponds to impaired emotion regulation.
“The prevailing neurobiological model of anxiety disorders posits that amygdala hyperreactivity to fearful or threatening stimuli is associated with heightened emotional reactivity, while disrupted processing in prefrontal regions is linked to impairments in emotional regulation (Berkman and Lieberman, 2009; Freitas-Ferrari et al., 2010; Kim et al., 2011).”
From Treatment for social anxiety disorder alters functional connectivity in emotion regulation neural circuitry (2017) · cites this paper as Freitas-Ferrari et al., 2010
Compared with healthy individuals, patients with social anxiety disorder show disrupted activation in the amygdala and prefrontal cortex.
“patients with SAD show: i) disrupted activation in the amygdala and regions of the prefrontal cortex (for reviews, see Berkman and Lieberman, 2009; Freitas-Ferrari et al., 2010; Kim et al., 2011)”
From Neural connectivity during affect labeling predicts treatment response to psychological therapies for social anxiety disorder. (2019) · cites this paper as Freitas-Ferrari et al., 2010
Converging lines of evidence from neuroimaging and pharmacological studies support the importance of glutamate abnormalities in the pathogenesis of SAD.
“Converging lines of evidence from neuroimaging and pharmacological studies support the importance of glutamate abnormalities in the pathogenesis of SAD (Freitas-Ferrari et al, 2010).”
From Ketamine for Social Anxiety Disorder: A Randomized, Placebo-Controlled Crossover Trial (2018) · cites this paper as Freitas-Ferrari et al, 2010
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References 130 · Cited by 298
Research works printed but not linked: 3
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- Authors
- Freitas-Ferrari, M. C., Hallak, J. E. C., Trzesniak, C., Filho, A. S., Machado-de-Sousa, J. P., Chagas, M. H. N., Nardi, A. E., & Crippa, J. A. S.
- Affiliations
- Universidade de São Paulo (BR)
- Corresponding author
- Crippa, José Alexandre S.
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 34
- Issue
- 4
- Pages
- 565-580
- ISSN
- 0278-5846 (ISSN-L)
- OpenAlex
- W2007223755
- Cited by
- 298
- References
- 130
- Citations by year
- 2026: 8 · 2025: 18 · 2024: 14 · 2023: 7 · 2022: 23 · 2021: 11 · 2020: 13 · 2019: 10 · 2018: 18 · 2017: 18 · 2016: 24 · 2015: 32 · 2014: 29 · 2013: 30 · 2012: 22
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fundação de Amparo à Pesquisa do Estado de São Paulo
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Universidade de São Paulo
- Fundação de Apoio ao Ensino, Pesquisa e Assistência do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- social anxiety disorder, neuroimaging, amygdala, limbic system, medial prefrontal cortex, dopamine, serotonin, facial emotion recognition, cerebral perfusion, treatment response, pathophysiology
- MeSH terms
- Brain, Brain Mapping, Magnetic Resonance Imaging, Phobic Disorders, Tomography, Emission-Computed, Single-Photon
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