***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: R and omized controlled trials have yielded promising results for internet-delivered cognitive behavior therapy ( iCBT ) for patients with social anxiety disorder ( SAD ) . The present study investigated anxiety-related neural changes after iCBT  for SAD . The amygdala is a critical hub in the neural fear network , receptive to change using emotion regulation strategies and a putative target for iCBT .  Twenty-two subjects were included in pre- and post-treatment functional magnetic resonance imaging at 3 T assessing neural changes during an affective face processing task . Treatment outcome was assessed using social anxiety self-reports and the Clinical Global Impression-Improvement ( CGI-I ) scale .  ICBT yielded better outcome than ABM ( 66 % vs. 25 % CGI-I responders ) . A significant differential activation of the left amygdala was found with relatively decreased reactivity after iCBT . Changes in the amygdala were related to a behavioral measure of social anxiety . Functional connectivity analysis in the iCBT group showed that the amygdala attenuation was associated with increased activity in the medial orbitofrontal cortex and decreased activity in the right ventrolateral and dorsolateral ( dlPFC ) cortices . Treatment-induced neural changes with iCBT were consistent with previously reported studies on regular CBT and emotion regulation in general Patients with anxiety disorders exhibit excessive neural reactivity in the amygdala , which can be normalized by effective treatment like cognitive behavior therapy ( CBT ) . Mechanisms underlying the brain ’s adaptation to anxiolytic treatments are likely related both to structural plasticity and functional response alterations , but multimodal neuroimaging studies addressing structure – function interactions are currently missing . Here , we examined treatment-related changes in brain structure ( gray matter ( GM ) volume ) and function ( blood – oxygen level dependent , BOLD response to self-referential criticism ) in 26 participants with social anxiety disorder r and omly assigned either to CBT or an attention bias modification control treatment . Also , 26 matched healthy controls were included . Significant time × treatment interactions were found in the amygdala with decreases both in GM volume ( family-wise error ( FWE ) corrected PFWE=0.02 ) and BOLD responsivity ( PFWE=0.01 ) after successful CBT . Before treatment , amygdala GM volume correlated positively with anticipatory speech anxiety ( PFWE=0.04 ) , and CBT-induced reduction of amygdala GM volume ( pre – post ) correlated positively with reduced anticipatory anxiety after treatment ( PFWE⩽0.05 ) . In addition , we observed greater amygdala neural responsivity to self-referential criticism in socially anxious participants , as compared with controls ( PFWE=0.029 ) , before but not after CBT . Further analysis indicated that diminished amygdala GM volume mediated the relationship between decreased neural responsivity and reduced social anxiety after treatment ( P=0.007 ) . Thus , our results suggest that improvement-related structural plasticity impacts neural responsiveness within the amygdala , which could be essential for achieving anxiety reduction with CBT Background Amygdala is considered as the core pathogenesis of generalized social anxiety disorder ( GSAD ) . However , it is still unclear whether effective group cognitive behavioral therapy ( CBT ) could modulate the function of amygdala-related network . We aim ed to examine the resting-state functional connectivity ( rsFC ) of the amygdala before and after group CBT . Methods Fifteen patients with GSAD were scanned on a 3 T MR system before and after 8 weeks of group CBT . For comparison , nineteen healthy control participants also underwent baseline fMRI scanning . We used bilateral amygdala as seed regions and the rsFC maps of the right and left amygdala were created separately in a voxel-wise way . Clusters survived two-tailed Gaussian R and om Field ( GRF ) correction at p < 0.05 ( voxel z value > 2.3 ) . Results Compared with baseline , patients with CBT showed significantly decreased connectivity of the left amygdala with the right putamen , the left dorsal medial prefrontal cortex ( dmPFC ) and the right dorsal anterior cingulate cortex ( dACC ) . Especially , the changes of the connectivity between the left amygdala and the dACC positively correlated with changes of the anxiety symptom in patients . Furthermore , in relative to controls , patients showed higher connectivity of left amygdala with dmPFC and dACC at baseline , while normal after CBT . Conclusions Short-term group CBT could down-regulate the abnormal higher connectivity of prefrontal-amygdala network , along with clinical improvement . This may provide a potential biomarker to monitor the treatment effect of CBT in GSAD patients Social anxiety disorder ( SAD ) is characterized at a neurobiological level by disrupted activity in emotion regulation neural circuitry . Previous work has demonstrated amygdala hyperreactivity and disrupted prefrontal responses to social cues in individuals with SAD ( Kim et al. , 2011 ) . While exposure-based psychological treatments effectively reduce SAD symptoms , not all individuals respond to treatment . Better underst and ing of the neural mechanisms involved offers the potential to improve treatment efficacy . In this study , we investigated functional connectivity in emotion regulation neural circuitry in a r and omized controlled treatment trial for SAD . Participants with SAD underwent fMRI scanning while performing an implicit emotion regulation task prior to  treatment ( n=62 ) . Following 12 weeks of cognitive behavioral therapy , acceptance and commitment therapy , or wait-list , participants completed a second scan ( n=42 ) . Psychophysiological interaction analyses using amygdala seed regions demonstrated differences between SAD and healthy control participants ( HC ; n=16 ) in right amygdala-vmPFC connectivity . SAD participants demonstrated more negative amygdala-to-vmPFC connectivity , compared to HC participants , an effect that was correlated with SAD symptom severity . Post-treatment symptom reduction was correlated with altered amygdala-to-vm/vlPFC connectivity , independent of treatment type . Greater symptom reduction was associated with more negative amygdala-to-vm/vlPFC connectivity . These findings suggest that effective psychological treatment for SAD enhances amygdala-prefrontal functional connectivity Background : Cognitive behavioral therapy ( CBT ) is an effective treatment for panic disorder with agoraphobia ( PD/AG ) . It is unknown , how variants of CBT differentially modulate brain networks involved in PD/AG . This study was aim ed to evaluate the effects of therapist-guided ( T+ ) versus self-guided ( T- ) exposure on the neural correlates of fear conditioning in PD/AG . Method : In a r and omized , controlled multicenter clinical trial in medication-free patients with PD/AG who were treated with 12 sessions of manualized CBT , functional magnetic resonance imaging ( fMRI ) was used during fear conditioning before ( t1 ) and after CBT ( t2 ) . Quality -controlled fMRI data from 42 patients and 42 healthy subjects ( HS ) were obtained . Patients were r and omized to two variants of CBT ( T+ , n = 22 , and T- , n = 20 ) . Results : The interaction of diagnosis ( PD/AG , HS ) , treatment group ( T+ , T- ) , time point ( t1 , t2 ) and stimulus type ( conditioned stimulus : yes , no ) revealed activation in the left hippocampus and the occipitotemporal cortex . The T+ group demonstrated increased activation of the hippocampus at t2 ( t2 > t1 ) , which was positively correlated with treatment outcome , and a decreased connectivity between the left inferior frontal gyrus and the left hippocampus across time ( t1 > t2 ) . Conclusion : After T+ exposure , contingency-encoding processes related to the posterior hippocampus are augmented and more decoupled from processes of the left inferior frontal gyrus , previously shown to be dysfunctionally activated in PD/AG . Linking single procedural variants to neural substrates offers the potential to inform about the optimization of targeted psychotherapeutic interventions BACKGROUND Neurofunctional changes underlying effective antianxiety treatments are incompletely characterized . This study explored the effects of citalopram and cognitive-behavioral therapy on regional cerebral blood flow ( rCBF ) in social phobia . METHODS By means of positron emission tomography with oxygen 15-labeled water , rCBF was assessed in 18 previously untreated patients with social phobia during an anxiogenic public speaking task . Patients were matched for sex , age , and phobia severity , based on social anxiety question naire data , and r and omized to citalopram medication , cognitive-behavioral group therapy , or a waiting-list control group . Scans were repeated after 9 weeks of treatment or waiting time . Outcome was assessed by subjective and psychophysiological state anxiety measures and self-report question naires . Questions were readministered after 1 year . RESULTS Symptoms improved significantly and roughly equally with citalopram and cognitive-behavioral therapy , whereas the waiting-list group remained unchanged . Four patients in each treated group and 1 waiting-list patient were classified as responders . Within both treated groups , and in responders regardless of treatment approach , improvement was accompanied by a decreased rCBF-response to public speaking bilaterally in the amygdala , hippocampus , and the periamygdaloid , rhinal , and parahippocampal cortices . Between-group comparisons confirmed that rCBF in these regions decreased significantly more in treated groups than control subjects , and in responders than nonresponders , particularly in the right hemisphere . The degree of amygdalar-limbic attenuation was associated with clinical improvement a year later . CONCLUSIONS Common sites of action for citalopram and cognitive-behavioral treatment of social anxiety were observed in the amygdala , hippocampus , and neighboring cortical areas , ie , brain regions subserving bodily defense reactions to threat The 16-item Quick Inventory of Depressive Symptomatology ( QIDS ) , a new measure of depressive symptom severity derived from the 30-item Inventory of Depressive Symptomatology ( IDS ) , is available in both self-report ( QIDS-SR(16 ) ) and clinician-rated ( QIDS-C(16 ) ) formats . This report evaluates and compares the psychometric properties of the QIDS-SR(16 ) in relation to the IDS-SR(30 ) and the 24-item Hamilton Rating Scale for Depression ( HAM-D(24 ) ) in 596 adult out patients treated for chronic nonpsychotic , major depressive disorder .  Internal consistency was high for the QIDS-SR(16 ) ( Cronbach 's alpha = .86 ) , the IDS-SR(30 ) ( Cronbach 's alpha = .92 ) , and the HAM-D(24 ) ( Cronbach 's alpha = .88 ) .  QIDS-SR(16 ) total scores were highly correlated with IDS-SR(30 ) ( .96 ) and HAM-D(24 ) ( .86 ) total scores . Item-total correlations revealed that several similar items were highly correlated with both QIDS-SR(16 ) and  IDS-SR(30 ) total scores . Roughly 1.3 times the QIDS-SR(16 )  total score is predictive of the HAM-D(17 ) ( 17-item version of the HAM-D ) total score . The QIDS-SR(16 ) was as sensitive to symptom change as the IDS-SR(30 ) and HAM-D(24 ) , indicating high concurrent validity for all three scales . The QIDS-SR(16 ) has highly acceptable psychometric properties , which supports the usefulness of this brief rating of depressive symptom severity in both clinical and research setting Background : The present study examined the prevalence of  social phobia  in the Swedish general population and demographic characteristics associated with this anxiety disorder . Methods : Data were obtained by means of a postal survey administrated to 2000 r and omly selected adults . A question naire , vali date d against clinical interviews and established social phobia scales , was used to assess social distress in a broad range of phobic situations , as well as the diagnostic criteria for social phobia corresponding to DSM-IV . Interpretable question naires were obtained from 1202 respondents ( 60.1 % ) . Results : The point prevalence of social phobia  was estimated at 15.6 % , but prevalence rates varied between 1.9 and 20.4 % across the different levels of distress and impairment used to define cases . Public speaking was the most common social fear . Social phobia was associated with female gender , low educational attainment , psychiatric medication use , and lack of social support . Conclusions : Although the exact diagnostic boundaries for social phobia are difficult to determine , it can be concluded that social anxiety is a distressing problem for a considerable proportion of the general population BACKGROUND Learning by conditioning is a key ability of animals and humans for acquiring novel behavior necessary for survival in a changing environment . Aberrant conditioning has been considered a crucial factor in the etiology and maintenance of panic disorder with agoraphobia ( PD/A ) . Cognitive-behavioral therapy ( CBT ) is an effective treatment for PD/A. However , the neural mechanisms underlying the effects of CBT on conditioning processes in PD/A are unknown . METHODS In a r and omized , controlled , multicenter clinical trial in medication-free patients with PD/A who were treated with 12 sessions of manualized CBT , functional magnetic resonance imaging ( fMRI ) was used during fear conditioning before and after CBT . Quality -controlled f 
    Output:
    
Conclusion : Neuroimaging studies suggest that abnormalities in hippocampus , amygdala , iFG , uncus and areas linked with emotional regulation ( dlPFC and ACC ) , predict a good outcome to  psychotherapy  in anxiety disorders .
HighlightsNeuroimaging studies suggest that hippocampus , amygdala , iFG , uncus dlPFC and ACC predict a good outcome to  psychotherapy  in anxiety disorders