Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI.
A characterizing symptom of social anxiety disorder (SAD) is increased emotional reactivity towards potential social threat in combination with impaired emotion and stress regulation. While several neuroimaging studies have linked SAD with hyperreactivity in limbic brain regions when exposed to emot...
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Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0050050&type=printable |
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| author | Ronald Sladky Anna Höflich Jacqueline Atanelov Christoph Kraus Pia Baldinger Ewald Moser Rupert Lanzenberger Christian Windischberger |
| author_facet | Ronald Sladky Anna Höflich Jacqueline Atanelov Christoph Kraus Pia Baldinger Ewald Moser Rupert Lanzenberger Christian Windischberger |
| author_sort | Ronald Sladky |
| collection | DOAJ |
| description | A characterizing symptom of social anxiety disorder (SAD) is increased emotional reactivity towards potential social threat in combination with impaired emotion and stress regulation. While several neuroimaging studies have linked SAD with hyperreactivity in limbic brain regions when exposed to emotional faces, little is known about habituation in both the amygdala and neocortical regulation areas. 15 untreated SAD patients and 15 age- and gender-matched healthy controls underwent functional magnetic resonance imaging during repeated blocks of facial emotion ([Formula: see text]) and object discrimination tasks ([Formula: see text]). Emotion processing networks were defined by a task-related contrast ([Formula: see text]). Linear regression was employed for assessing habituation effects in these regions. In both groups, the employed paradigm robustly activated the emotion processing and regulation network, including the amygdalae and orbitofrontal cortex (OFC). Statistically significant habituation effects were found in the amygdalae, OFC, and pulvinar thalamus of SAD patients. No such habituation was found in healthy controls. Concurrent habituation in the medial OFC and the amygdalae of SAD patients as shown in this study suggests intact functional integrity and successful short-term down-regulation of neural activation in brain areas responsible for emotion processing. Initial hyperactivation may be explained by an insufficient habituation to new stimuli during the first seconds of exposure. In addition, our results highlight the relevance of the orbitofrontal cortex in social anxiety disorders. |
| format | Article |
| id | doaj-art-45fd42d1d196432caa352f4ecf0419ab |
| institution | OA Journals |
| issn | 1932-6203 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-45fd42d1d196432caa352f4ecf0419ab2025-08-20T02:30:39ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-01711e5005010.1371/journal.pone.0050050Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI.Ronald SladkyAnna HöflichJacqueline AtanelovChristoph KrausPia BaldingerEwald MoserRupert LanzenbergerChristian WindischbergerA characterizing symptom of social anxiety disorder (SAD) is increased emotional reactivity towards potential social threat in combination with impaired emotion and stress regulation. While several neuroimaging studies have linked SAD with hyperreactivity in limbic brain regions when exposed to emotional faces, little is known about habituation in both the amygdala and neocortical regulation areas. 15 untreated SAD patients and 15 age- and gender-matched healthy controls underwent functional magnetic resonance imaging during repeated blocks of facial emotion ([Formula: see text]) and object discrimination tasks ([Formula: see text]). Emotion processing networks were defined by a task-related contrast ([Formula: see text]). Linear regression was employed for assessing habituation effects in these regions. In both groups, the employed paradigm robustly activated the emotion processing and regulation network, including the amygdalae and orbitofrontal cortex (OFC). Statistically significant habituation effects were found in the amygdalae, OFC, and pulvinar thalamus of SAD patients. No such habituation was found in healthy controls. Concurrent habituation in the medial OFC and the amygdalae of SAD patients as shown in this study suggests intact functional integrity and successful short-term down-regulation of neural activation in brain areas responsible for emotion processing. Initial hyperactivation may be explained by an insufficient habituation to new stimuli during the first seconds of exposure. In addition, our results highlight the relevance of the orbitofrontal cortex in social anxiety disorders.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0050050&type=printable |
| spellingShingle | Ronald Sladky Anna Höflich Jacqueline Atanelov Christoph Kraus Pia Baldinger Ewald Moser Rupert Lanzenberger Christian Windischberger Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI. PLoS ONE |
| title | Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI. |
| title_full | Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI. |
| title_fullStr | Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI. |
| title_full_unstemmed | Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI. |
| title_short | Increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by FMRI. |
| title_sort | increased neural habituation in the amygdala and orbitofrontal cortex in social anxiety disorder revealed by fmri |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0050050&type=printable |
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