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Cited by 65Anxiety, Depression, Psychometrics, Treatment, Cognitive ProcessesFunctional Brain Connectivity StudiesNeural and Behavioral Psychology Studies

Treatment for social anxiety disorder alters functional connectivity in emotion regulation neural circuitry

Open access
Young, Katherine S., Burklund, Lisa J., Torre, Jared B., Saxbe, Darby, Lieberman, Matthew D., Craske, Michelle G.·2017·Psychiatry Research - Neuroimaging
DOI 10.1016/j.pscychresns.2017.01.005PMC PMC5330298
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Abstract

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 understanding 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 randomized 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. © 2017 Elsevier Ireland Ltd

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Crossref · 10.1016/j.pscychresns.2017.01.005

Cites

53 of 53 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

28 of 68 cited sources checked · 18 supported · 1 flagged · accuracy not yet measured

  • Premisecitation

    When task demands are low, individuals with social anxiety disorder show heightened amygdala reactivity compared to healthy individuals.

    “when task demands are minimal, amygdala reactivity was found to be heightened in individuals with SAD, relative to healthy individuals”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Burklund et al., 2015 source

      The Discussion (page unavailable) says that none of the social phobia groups showed greater amygdala activity than healthy controls during the emotion-reactivity affect-matching task. Although the Introduction describes heightened reactivity as an expectation based on earlier research, this study reports no group difference in that task. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
  • Premisecitation

    Across studies, a general pattern emerges of disrupted prefrontal activity in individuals with social anxiety disorder compared to healthy controls when they are explicitly instructed to use a regulatory strategy.

    “Across these studies, there is a general trend for disrupted (increased or decreased) levels of activity in prefrontal regions (dorsolateral and ventrolateral prefrontal cortex, dl/vlPFC, dorsal anterior cingulate cortex, dACC) among individuals with SAD, relative to healthy control participants when explicitly instructed to engage in a regulatory strategy (for recent meta-analyses, see Brühl et”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites Brühl et al., 2014

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Zilverstand et al., 2016 source

      The Results (§3, §3.2) include five social anxiety disorder studies and report altered dlPFC, vlPFC, and dACC activity during cognitive reappraisal compared with healthy controls, including one study with increased dlPFC activity. However, the reported cross-study pattern is for anxiety disorders as a group, not specifically for social anxiety disorder; the paper does not establish that the same pattern holds across the SAD studies alone. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Findingown data

    CBT and ACT did not differ significantly in symptom reduction.

    “no significant difference between CBT and ACT (p = .81), also consistent with [3].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [3] Berkman, 2009, Using Neuroscience To Broaden Emotion Regulation: theoretical and methodological considerations, Soc. Pers. Psychol. Compass source

      The Review of Neuroscience Investigations of Emotion Regulation compares reappraisal with suppression, while the Broadening Emotion Regulation section discusses how few studies compare regulation strategies. Neither section reports a CBT-versus-ACT symptom-reduction comparison or a p-value of .81 (searched for CBT, ACT, their full names, and the reported p-value). (LLM, conf=0.76)

      Experimental — accuracy not yet measured
  • Premisecitation

    At the neurobiological level, social anxiety disorder involves disrupted activity in the neural circuitry for emotion regulation.

    “Social anxiety disorder (SAD) is characterized at a neurobiological level by disrupted activity in emotion regulation neural circuitry.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Kim et al., 2011 source
  • Study design and conductown data

    Before treatment, LSAS-SR scores did not differ significantly by treatment group (CBT, ACT, or WL).

    “A one-way ANOVA confirmed no significant differences in LSAS-SR score based on allocation of treatment group (CBT, ACT or WL; F(2, 61) = 2.52, p = .09) prior to beginning of treatment, consistent with results for the full sample of the parent study [3].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [3] Berkman, 2009, Using Neuroscience To Broaden Emotion Regulation: theoretical and methodological considerations, Soc. Pers. Psychol. Compass source

      The Review of Neuroscience Investigations of Emotion Regulation discusses neural responses to regulation strategies, not baseline scores in a treatment trial. Searches for LSAS-SR, CBT, ACT, waitlist allocation, and baseline group differences found no passage addressing the claimed comparison. Page numbers were not available in our copy. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim. 37
  • May combine two claims. 26

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Affect labeling is frequently used in laboratory research on emotion regulation because it allows measurement of activation in emotion regulation circuitry without requiring the effort or intentionality typical of voluntary regulation.

    “It is commonly used in the laboratory to investigate emotional regulation as it provides a way to measure activation in emotion regulation circuitry independent of the effort or intentionality that is typically required to engage in voluntary regulation (Creswell et al., 2007; Lieberman et al., 2007; Payer et al., 2012).”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites Creswell et al., 2007 source
    • cites Lieberman et al., 2007 source
    • cites Payer et al., 2012 source

  • May combine two claims.

    Premisecitation

    Previous functional connectivity studies have found that while viewing faces, greater social anxiety disorder symptom severity was associated with greater connectivity between the amygdala and fusiform gyrus and between the amygdala and superior temporal sulcus.

    “Previous functional connectivity studies have shown that while viewing face stimuli, greater SAD symptom severity was associated with greater amygdala to fusiform gyrus and amygdala to superior temporal sulcus connectivity in one study (Frick et al., 2013)”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Frick et al., 2013 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    There is no significant difference in right ventrolateral prefrontal cortex activity during implicit emotion regulation between individuals with social anxiety disorder and healthy individuals.

    “but there was no significant difference in right vlPFC activity during implicit emotion regulation (Burklund et al., 2015).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Burklund et al., 2015 source

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    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).”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites Berkman and Lieberman, 2009 source

      The Conclusion (page not provided) describes prefrontal involvement in down-regulating the amygdala, and the review section reports greater prefrontal and lower amygdala activity during reappraisal. These passages support the general emotion-regulation circuitry, but they do not present it as the prevailing model of anxiety disorders or establish amygdala hyperreactivity and disrupted prefrontal processing in those disorders. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites Freitas-Ferrari et al., 2010 source
    • cites Kim et al., 2011 source

  • May combine two claims.

    Premisecitation

    However, the findings are not fully consistent, as two recent studies found no significant differences in prefrontal activity during regulation between social anxiety disorder and healthy control groups.

    “However, findings are not entirely consistent, with two recent studies demonstrated no significant differences in prefrontal activity during regulation between groups of SAD and healthy control participants (Burklund et al., 2015; Gaebler et al., 2014).”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites Burklund et al., 2015 source
    • cites Gaebler et al., 2014 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductcitation

    Therapy for both treatment conditions followed detailed treatment manuals for anxiety.

    “Therapy for both treatment conditions was based on detailed treatment manuals for anxiety (CBT (Hope et al., 2000), ACT (Eifert and Forsyth, 2005); see (Craske et al., 2014) for full details).”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites Hope et al., 2000

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Eifert and Forsyth, 2005

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Craske et al., 2014 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Affect labeling is regarded as an incidental or implicit form of emotion regulation.

    “Affect labeling, the act of putting feelings into words, is considered an ‘incidental’ or ‘implicit’ form of emotion regulation”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites Kircanski et al., 2012 source
    • cites Lieberman et al., 2011 source

      The General Discussion section, “Affect Labeling as Incidental Emotion Regulation,” describes affect labeling as incidental emotion regulation. It explicitly prefers “incidental” over “implicit,” however, because people are aware that they are labeling their feelings. (LLM, conf=0.92)

      Experimental — accuracy not yet measured
    • cites Niles et al., 2015 source

  • May combine two claims.

    Premisecitation

    Exposure-based psychological treatments are effective at reducing social anxiety disorder symptoms, but a portion of individuals do not respond.

    “While exposure-based psychological treatments effectively reduce SAD symptoms, not all individuals respond to treatment.”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites Craske et al., 2014 source
    • cites Rodebaugh et al., 2004 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Affect labeling has been demonstrated to be an effective regulatory strategy that reduces the intensity of emotional reactions to labeled stimuli.

    “has been shown to be an effective regulatory strategy, diminishing the intensity of emotional reactions to labeled stimuli (Kircanski et al., 2012; Lieberman et al., 2011; Niles et al., 2015; Tabibnia et al., 2008).”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites Kircanski et al., 2012 source
    • cites Lieberman et al., 2011 source
    • cites Niles et al., 2015 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Another study found that greater social anxiety disorder symptom severity was associated with connectivity between the amygdala and dorsal anterior cingulate cortex/dorsal medial prefrontal cortex.

    “or amygdala to dACC/dorsal medial PFC connectivity in another (Demenescu et al., 2013).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Demenescu et al., 2013 source

      The Results (section 3.3, p. 5) report that greater anxiety symptom severity correlated with stronger left amygdala–right rostral ACC and left amygdala–dorsal mPFC connectivity during fearful-face perception. The finding was measured across anxiety patients, including those with panic disorder, rather than specifically as a relationship with social anxiety disorder symptom severity. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Earlier research has shown that people with social anxiety disorder have heightened amygdala reactivity and altered prefrontal responses to social cues.

    “Previous work has demonstrated amygdala hyperreactivity and disrupted prefrontal responses to social cues in individuals with SAD (Kim et al., 2011).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Kim et al., 2011 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Both explicit and incidental emotion regulation have been shown to increase prefrontal cortex activity and decrease amygdala activity in healthy individuals.

    “Both explicit and incidental forms of emotion regulation have been shown to increase PFC and decrease amygdala activity in healthy participants (Burklund et al., 2014; Delgado et al., 2008; Hariri et al., 2000; Lieberman et al., 2007; Ochsner et al., 2002).”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites Burklund et al., 2014 source
      Experimental — accuracy not yet measured
    • cites Delgado et al., 2008 source
    • cites Hariri et al., 2000 source

  • May combine two claims.

    Premisecitation

    Two studies comparing cognitive behavioral therapy to wait-list groups of social anxiety disorder patients found treatment-related increases in inverse connectivity between dorsomedial prefrontal cortex and left amygdala during reappraisal of negative self-beliefs, and positive connectivity among prefrontal regions during reappraisal of social criticism.

    “Two studies comparing CBT to wait-list groups of SAD patients demonstrated treatment-related increases in i) inverse connectivity between the dmPFC and left amygdala while reappraising negative self-beliefs (Goldin et al., 2013), and ii) positive connectivity among prefrontal regions including medial PFC, dmPFC, left dACC, left dlPFC and left vlPFC when reappraising social criticism (Goldin et al.”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites Goldin et al., 2013 source
    • cites Goldin et al., 2014 source

      Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Psilocybin administration reduces top-down connectivity from the amygdala to primary visual cortex.

    “psilocybin administration reduced top-down amygdala to primary visual connectivity (Kraehenmann et al., 2016).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Kraehenmann et al., 2016 source

      The Discussion reports that psilocybin, compared with placebo, reduced the effect of visual threat on the top-down connection from the amygdala to V1 (primary visual cortex). The citing sentence omits that qualification: the paper does not establish a general reduction in amygdala-to-V1 connectivity outside threat processing. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Recent work found marked differences in neural activity during affect labeling in individuals with comorbid depression.

    “Recent work has demonstrated marked differences in neural activity associated with affect labeling in individuals with comorbid depression (Burklund et al., 2014).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Burklund et al., 2014 source

      The Discussion (page unavailable) reports neural activity associated with affect labeling, including differences from reappraisal. But the Methods > Participants section (page unavailable) describes a healthy older-adult sample, not individuals with comorbid depression; the claimed population is unsupported. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Affect labeling was found to increase inverse connectivity from right vlPFC to amygdala in healthy adults.

    “while affect labeling was found to specifically increase inverse connectivity from right vlPFC to amygdala in healthy adults (Torrisi et al., 2013).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Torrisi et al., 2013 source

  • May combine two claims.

    Findingown data

    Reduction in symptoms after treatment was associated with changes in connectivity between the amygdala and ventromedial/ventrolateral prefrontal cortex, and this association did not depend on which treatment was received.

    “Post-treatment symptom reduction was correlated with altered amygdala-to-vm/vlPFC connectivity, independent of treatment type.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    With the right amygdala seed, post-hoc pairwise comparison found one significant cluster for WL > CBT in inferior temporal gyrus and no clusters for CBT > WL.

    “Post-hoc pairwise comparisons using the right amygdala seed region demonstrated one significant cluster for WL > CBT, located in the inferior temporal gyrus (and no clusters for CBT > WL).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Participants with the greatest symptom reduction showed more negative amygdala-prefrontal connectivity, while those with less or no symptom reduction showed more positive connectivity.

    “While participants with greatest symptom reduction demonstrated more negative amygdala-prefrontal functional connectivity, participants with less or no symptom reduction demonstrated effects in the opposite direction (more positive amygdala-prefrontal connectivity).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    No significant functional connectivity differences were found between ACT and WL or between CBT and ACT using either left or right amygdala seeds.

    “There were no significant differences in functional connectivity using either the left or right amygdala as seed regions between groups of ACT vs. WL or CBT vs. ACT.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    With the left amygdala seed, post-hoc pairwise comparison found one significant cluster for WL > CBT in left dlPFC and no clusters for CBT > WL.

    “Using the left amygdala as seed region, there was one significant cluster for WL > CBT, located in the left dlPFC (and again no significant clusters for CBT > WL).”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Interpretationreasoning

    One possible explanation for this pattern is that dysregulated amygdala activity in social anxiety disorder during implicit emotion regulation results from disrupted functional connectivity between the amygdala and prefrontal cortex, rather than from a failure to activate prefrontal regions.

    “One explanation for this effect is that dysregulated amygdala activity in SAD during implicit emotion regulation may be attributable to disrupted communication, or functional connectivity, between amygdala and prefrontal cortex, rather than a failure to activate prefrontal regions per se.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    In contrast to the extensive research on emotional reactivity in social anxiety disorder, only a small number of studies have examined disruptions in emotion regulation.

    “Compared to the body of work investigating emotional reactivity in SAD, few studies have assessed disruptions in emotion regulation.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The model included motion parameters as regressors of no interest.

    “Motion parameters were included in the model as regressors of no interest.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Study design and conductown data

    Participants with social anxiety disorder were divided by age and gender and then randomly allocated to cognitive behavioral therapy, acceptance and commitment therapy, or wait list.

    “One hundred participants with SAD were stratified by age and gender and randomized to CBT (n = 40), ACT (n = 34), or wait list (WL; n = 26).”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductnone given

    All PPI analyses applied whole-brain correction for multiple comparisons with an alpha of 0.05, a voxelwise threshold of p<.005, a minimum cluster size of 40 voxels, two-tailed tests, and 3dClustSim in AFNI.

    “In all PPI analyses, whole-brain correction for multiple comparisons using an alpha level of 0.05 determined a voxelwise threshold of p<.005 combined with a minimum cluster size of 40 voxels (two-tailed tests; 3dClustSim, AFNI).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductreasoning

    A small volume correction was applied to amygdala reactivity analyses due to strong prior hypotheses about amygdala function.

    “Given strong a priori hypotheses regarding the functioning of the amygdala, a small volume correction was used to assess changes in amygdala reactivity.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    In a study of internet-delivered cognitive behavioral therapy for social anxiety disorder, treatment-related reductions in amygdala reactivity to affective faces were associated with increased medial orbitofrontal cortex activity and decreased ventral and dorsal lateral prefrontal cortex activity.

    “In a study of internet-delivered CBT (iCBT) for SAD, treatment-related reductions in amygdala reactivity to affective faces were associated with i) increases in mOFC activity (i.e., inverse connectivity) and ii) decreases in ventral and dorsal lateral PFC activity (i.e., positive connectivity) (Månsson et al., 2013).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Månsson et al., 2013 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Cognitive behavioral therapy teaches reappraisal, which is the intentional re-framing of negative or unpleasant thoughts or experiences.

    “CBT teaches ‘reappraisal’, the intentional re-framing of negative or unpleasant thoughts or experiences (Craske, 2010).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Craske, 2010

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The magnitude of amygdala reactivity has been shown to correlate with the severity of social anxiety disorder symptoms.

    “the extent of which has been shown to correlate with symptom severity (Cooney et al., 2006; Goldin et al., 2009b; Phan et al., 2006; Shah and Angstadt, 2009).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Cooney et al., 2006 source
    • cites Goldin et al., 2009b

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Phan et al., 2006 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The order of conditions was counterbalanced across participants.

    “Condition order was counterbalanced across participants.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductcitation

    The LSAS-SR has been reported to have high reliability and validity.

    “SAD severity was assessed using the Liebowitz Social Anxiety Scale–Self-Report Version (LSAS-SR, a measure with high reliability and validity; Baker et al., 2002; Fresco et al., 2001).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Baker et al., 2002 source
    • cites Fresco et al., 2001 source

  • Classified as probably not a substantial claim.

    Study design and conductown data

    We corrected for multiple comparisons with 3dClustStim, a Monte Carlo simulation tool.

    “Multiple comparison correction was performed using 3dClustStim (AFNI: http://afni.nimh.nih.gov/afni/), which conducts a Monte Carlo simulation.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Acceptance and commitment therapy promotes acceptance, which involves acknowledging that emotional experiences are fleeting and can be viewed with perspective.

    “ACT promotes ‘acceptance’, the acknowledgement that emotional experiences are fleeting and can be viewed with a sense of perspective (Hayes et al., 1999).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Hayes et al., 1999

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Only participants who completed all 12 treatment sessions, i.e., full compliance, were included in the analyses.

    “Only participants with full treatment compliance (i.e. completed all 12 sessions of treatment) were included in the reported analyses.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Ketamine administration modulates connectivity between the amygdala and pregenual anterior cingulate cortex.

    “ketamine administration was found to modulate connectivity between amygdala and pregenual anterior cingulate cortex (Scheidegger et al., 2016)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Scheidegger et al., 2016 source

  • Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).

    Interpretationcitation

    It is plausible that comorbidities similarly affect changes in functional connectivity.

    “It is plausible that comorbidities similarly impact changes in functional connectivity.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Recent studies show that psychotropic medications given to healthy volunteers can affect amygdala functional connectivity, with different substances affecting different regions.

    “recent studies have demonstrated that administration of psychotropic medications in healthy volunteers can impact amygdala functional connectivity, with different substances affecting connectivity with different regions.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Medial PFC regions are broadly considered to support autonomous emotion regulation, while lateral PFC regions are thought necessary for cognitive reappraisal and voluntary downregulation.

    “Medial regions of PFC are broadly considered to be recruited for autonomous emotion regulation while lateral regions are thought to be necessary for cognitive reappraisal and voluntary downregulation (Ochsner and Gross, 2005; Phillips et al., 2008).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites Ochsner and Gross, 2005 source
    • cites Phillips et al., 2008 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    These emotion regulation systems are widely regarded as reciprocally linked and acting together to support voluntary and automatic processing of emotional stimuli.

    “These systems are, however, widely regarded to be reciprocally linked, acting in concert to support voluntary and automatic processing and reactions to emotional stimuli (Phillips et al., 2008).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Phillips et al., 2008 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Interpretationnone given

    Participant attrition is a major challenge in multi-visit studies like this one, and high anxiety may have contributed to greater motion during scans.

    “Participant attrition is a major challenge in multi-visit studies such as that described here and high levels of anxiety in subjects may have additionally contributed to greater amounts of motion during scans.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    Treatment-related symptom reduction might act through compensatory mechanisms that alter engagement of both medial incidental and lateral voluntary emotion regulation regions.

    “Treatment-related symptom reduction might be thought to act through compensatory mechanisms, altering engagement of both medial ‘incidental’ and lateral ‘voluntary’ emotion regulation regions.”
    Quote in the paperNot a substantial claim
    • The authors state this as an assumption: Task-related changes in functional connectivity can be interpreted as regions working together to perform a task-related function.

  • May combine two claims.

    Study design and conductnone given

    PPI functional connectivity analyses are correlational and cannot establish directionality.

    “PPI functional connectivity analyses, however, are correlational in nature.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Interpretationreasoning

    If the functional separation between medial and lateral PFC holds, the findings suggest impaired neural circuitry for incidental emotion regulation during pre-treatment affect labeling.

    “Were this functional separation to hold true, findings presented here would suggest an impairment in neural circuitry supporting incidental emotion regulation during affect labeling pre-treatment.”
    Quote in the paperSubstantial claim
    • The authors state this as an assumption: Task-related changes in functional connectivity can be interpreted as regions working together to perform a task-related function.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Interpretationreasoning

    Different types of disrupted amygdala reactivity may constitute different neural profiles of SAD, which may have different patterns of prefrontal functional connectivity.

    “it is possible that different types of disrupted amygdala reactivity constitute different ‘neural profiles’ of SAD and in turn, might be characterized by different patterns of functional connectivity with prefrontal cortical regions.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Meta-analyses of explicit emotion regulation show that, compared with healthy adults, individuals with SAD have reduced lateral prefrontal activity and reduced inverse connectivity between those regions and the amygdala.

    “Compared to healthy adults, individuals with SAD had reduced activity in lateral prefrontal regions, as well as reduced inverse connectivity between these regions and the amygdala (see Brühl et al., 2014 for review).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Brühl et al., 2014

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Prior research describes several aspects of dysfunctional amygdala reactivity in SAD: a temporal delay, more sustained reactivity in learned fear, and over-generalization to non-threatening cues.

    “Prior research has described different aspects of dysfunctional amygdala reactivity including: a temporal delay in amygdala reactivity in SAD (Campbell et al., 2007); more sustained amygdala reactivity in learned fear responses (Andreatta et al., 2015); and over-generalization of amygdala reactivity to non-threatening cues (Cooney et al., 2006).”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Campbell et al., 2007 source
    • cites Andreatta et al., 2015 source
    • cites Cooney et al., 2006 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Administration of (S)-citalopram is associated with enhanced downregulation of the amygdala by orbitofrontal cortex.

    “Administration of (S)-citalopram was found to be associated with enhanced downregulation of amygdala by orbitofrontal cortex, as demonstrated using dynamic causal modeling (Sladky et al., 2015b)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Sladky et al., 2015b

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Interpretationown data

    Changes in amygdala-prefrontal connectivity depend on an individual's response to treatment, because the pattern appeared only when the symptom change covariate was included.

    “Notably, this pattern of effects was observed only with the inclusion of the symptom change covariate, suggesting that changes in amygdala-prefrontal connectivity are dependent upon an individual’s response to treatment.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Previous work suggests that task demands influence which prefrontal sub-regions are recruited for regulation, with explicit regulation implicating lateral PFC and implicit regulation involving medial PFC.

    “Previous work has suggested that differing task demands may influence the recruitment of different prefrontal sub-regions for regulatory purposes, i.e. during explicit regulation, lateral PFC regions may be implicated, while for more implicit regulation, medial PFC regions are involved (see Sladky et al., 2015a).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Sladky et al., 2015a

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    Affect labeling is considered an implicit or incidental regulation approach, but lateral prefrontal regions are typically recruited during it.

    “Although considered an implicit or ‘incidental’ regulation approach, recruitment of lateral prefrontal regions is typically observed (Lieberman et al., 2007).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Lieberman et al., 2007 source
51 of 51

  • The authors state this as an assumption.

    Task-related changes in functional connectivity can be interpreted as regions working together to perform a task-related function.

    “Task-specific changes in functional connectivity are subsequently interpreted as regions working in concert to achieve a task-related function.”
1 of 1

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In patients with SAD given CBT or ACT, how much their SAD improved was linked to amygdala-ventromedial prefrontal cortex connectivity after treatment.

    “Young and colleagues (2017) found that in a sample of patients with SAD who were assigned to cognitive behavior therapy (CBT) or acceptance and commitment therapy (ACT), degree of SAD reduction in treatment correlated with functional connectivity between the amygdala and ventromedial prefrontal cortex at post-treatment.”

    From Self-referential processing during observation of a speech performance task in social anxiety disorder from pre- to post-treatment: Evidence of disrupted neural activation (2019) · cites this paper as Young et al., 2017

    The Results (§3.4) and Discussion (§4.2) link greater SAD symptom reduction to a more negative *change from pre- to post-treatment* in left amygdala–vmPFC connectivity. They do not report the claimed correlation with connectivity measured only at post-treatment; the analysis was also independent of treatment group and included wait-list participants, not only those assigned CBT or ACT. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • In prior work by the authors, social anxiety disorder symptom reduction following cognitive behavioral therapy or acceptance and commitment therapy was associated with enhanced inverse connectivity between ventromedial/ventrolateral prefrontal cortex and amygdala during implicit emotion regulation.

    “In previous work, we demonstrated that enhanced inverse connectivity within this circuitry was associated with symptom reduction following treatment, collapsing across CBT and ACT groups (Young et al., 2017).”

    From Neural connectivity during affect labeling predicts treatment response to psychological therapies for social anxiety disorder. (2019) · cites this paper as Young et al., 2017

  • Functional connectivity studies report disrupted amygdala-prefrontal communication in SAD during rest, implicit emotion regulation, and explicit emotion regulation tasks.

    “Functional connectivity studies have found that compared to healthy individuals, individuals with SAD demonstrate disrupted communication between the amygdala and prefrontal regions during resting state (vmPFC (Hahn et al., 2011)), as well as during implicit (vmPFC (Young et al., 2017)) and explicit emotion regulation tasks (dl/vlPFC (Goldin et al., 2009)).”

    From Changes in functional connectivity with cognitive behavioral therapy for social anxiety disorder predict outcomes at follow-up (2020) · cites this paper as Young et al., 2017

  • Changes in this circuitry have been proposed as mechanisms of treatment response.

    “Changes in this circuitry have been implicated as mechanisms in treatment response (Goldin et al., 2013, 2014; Young et al., 2017).”

    From Changes in functional connectivity with cognitive behavioral therapy for social anxiety disorder predict outcomes at follow-up (2020) · cites this paper as Young et al., 2017

  • The present findings matched this framework except for vlPFC, which is traditionally found during affect labeling in healthy controls and was implicated in short-term treatment response in the authors' prior analyses.

    “Our findings were consistent with the exception of the vlPFC, which is traditionally found during affect labeling in healthy controls (Lieberman et al., 2007; Torre & Lieberman, 2018) and was implicated in short-term treatment response in our previous analyses (Young et al., 2017).”

    From Changes in functional connectivity with cognitive behavioral therapy for social anxiety disorder predict outcomes at follow-up (2020) · cites this paper as Young et al., 2017

Statistics recomputed

Every reported test result, recomputed from its test statistic and degrees of freedom. A result shows as not adding up only once an independent check has confirmed it.

  • ConsistentF(2, 61) = 2.52reported p = .09 · recomputed p = .089

    “F(2, 61) = 2.52, p = .09”

  • ConsistentF(2, 41) = 12.78reported p < .001 · recomputed p < .001

    “F(2, 41) = 12.78, p < .001”

2 of 2

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Baseline connectivity analysis exceeds the reported SAD sample

    Minor

    The abstract reports 62 SAD participants scanned before treatment, but the baseline amygdala-connectivity correlation reports 64 SAD participants. That analysis cannot include more SAD participants than the reported baseline scan sample.

  • Stated task duration exceeds the functional scan time

    Minor

    Four blocks of each of four conditions, with six five-second trials per block, require 480 seconds of trials. Even allowing only five ten-second intervals within each block adds 800 seconds, exceeding the 1,032 seconds supplied by 344 volumes at a three-second TR.

2 of 2

Cites

Flagged first, then by citations

1 of the 54 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Brown, 1994, Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV): client Interview Schedule, Graywind Publ. Inc.

Cited by

Sorted by citations

Related

Authors
Young, K. S., Burklund, L. J., Torre, J. B., Saxbe, D., Lieberman, M. D., & Craske, M. G.
Affiliations
  • University of California, Los Angeles (US)
  • University of Southern California (US)
Corresponding author
Craske, Michelle G.
ORCID
Venue
Psychiatry Research - Neuroimaging
Publisher
Elsevier BV
Published
2017-03
Volume
261
Pages
44-51
ISSN
0925-4927 (ISSN-L)
DOI
10.1016/j.pscychresns.2017.01.005
PMC
PMC5330298
OpenAlex
W2577085700
Cited by
64
References
54
Citations by year
2026: 3 · 2025: 4 · 2024: 5 · 2023: 7 · 2022: 4 · 2021: 7 · 2020: 12 · 2019: 8 · 2018: 13 · 2017: 1
FWCI
12.03
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Psychiatry Research Neuroimaging (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
National Institute of Mental Health (R21MH081299)
Topics
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Functional Brain Connectivity Studies
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
Keywords
social anxiety disorder, functional connectivity, amygdala, ventromedial prefrontal cortex, ventrolateral prefrontal cortex, emotion regulation, cognitive behavioral therapy, acceptance and commitment therapy, treatment response, symptom severity, psychophysiological interaction, implicit emotion regulation
MeSH terms
Phobia, Social, Adult, Amygdala, Emotions, Female, Humans, Magnetic Resonance Imaging, Male, Nerve Net, Cognitive Behavioral Therapy, Treatment Outcome, Young Adult, Acceptance and Commitment Therapy

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read under definition version 3 (extract-v3) on 2026-09-28.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-09-28.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

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