{"title":"Neuroimaging in anxiety disorders.","authors":"Mats Fredrikson, Vanda Faria","doi":"10.1159/000351938","DOIUrl":null,"url":null,"abstract":"<p><p>Neuroimaging studies using functional magnetic resonance imaging (fMRI), positron emission tomography (PET) and single-photon emission computed tomography (SPECT) to evaluate neurofunctional and neurochemical alterations related to the generation and control of affect in patients with anxiety disorders are reviewed. We performed a meta-analysis of symptom provocation studies, where neural activity was measured using fMRI, PET or SPECT to test the hypothesis that prefrontal regions modulate amygdala activity. Data revealed that reactivity in the amygdala was enhanced in patients with phobia as well as posttraumatic stress disorder (PTSD). The dorsal anterior cingulate cortex was activated in concert with the amygdala, both in PTSD and in phobic states, suggesting a role in fear expression, rather than emotional control. Activity in emotion-regulating areas in the ventromedial prefrontal cortex including the subgenual anterior cingulate cortex and the medial orbitofrontal cortex was compromised in the symptomatic state in PTSD and phobic disorders, respectively. Increased amygdala reactivity was restored with psychological treatment. Treatment effects across different modalities including pharmacological and psychological interventions as well as with placebo regimens support that reduction of neural activity in the amygdala may be a final common pathway for successful therapeutic interventions irrespective of method, thereby linking neurotransmission to plasticity in a pivotal node of the core fear network of the brain. </p>","PeriodicalId":74212,"journal":{"name":"Modern trends in pharmacopsychiatry","volume":"29 ","pages":"47-66"},"PeriodicalIF":0.0000,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000351938","citationCount":"21","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Modern trends in pharmacopsychiatry","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000351938","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/9/20 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 21
Abstract
Neuroimaging studies using functional magnetic resonance imaging (fMRI), positron emission tomography (PET) and single-photon emission computed tomography (SPECT) to evaluate neurofunctional and neurochemical alterations related to the generation and control of affect in patients with anxiety disorders are reviewed. We performed a meta-analysis of symptom provocation studies, where neural activity was measured using fMRI, PET or SPECT to test the hypothesis that prefrontal regions modulate amygdala activity. Data revealed that reactivity in the amygdala was enhanced in patients with phobia as well as posttraumatic stress disorder (PTSD). The dorsal anterior cingulate cortex was activated in concert with the amygdala, both in PTSD and in phobic states, suggesting a role in fear expression, rather than emotional control. Activity in emotion-regulating areas in the ventromedial prefrontal cortex including the subgenual anterior cingulate cortex and the medial orbitofrontal cortex was compromised in the symptomatic state in PTSD and phobic disorders, respectively. Increased amygdala reactivity was restored with psychological treatment. Treatment effects across different modalities including pharmacological and psychological interventions as well as with placebo regimens support that reduction of neural activity in the amygdala may be a final common pathway for successful therapeutic interventions irrespective of method, thereby linking neurotransmission to plasticity in a pivotal node of the core fear network of the brain.