|
| Diagnosis | Study | Number of patients (intervention group) | Design | Treatment effects of psychotherapy |
|
| PD | Kircher et al. (2013) | 42 (unmedicated) | fMRI
12 weeks of CBT | Normalization of hyperactivation in IFG. Greater connectivity between IFG and: amygdala, hippocampus, ACC, mPFC, and lPFC
Decrease in activation in the amygdala, anterior insula, dACC, rACC, and vmPFC |
| Lueken et al. (2013) | 49 (unmedicated) | fMRI
12 sessions of CBT (twice-weekly for six weeks) | Normalized hyperactivation of pgACC and amygdala. Increase in hippocampal activation with stimulus contingency processing
Enhanced ACC-amygdala coupling |
Straube et al. (2014)
[144] | 42 (unmedicated) | fMRI
12 sessions of manualized CBT
Patient-guided and therapist-guided protocols were compared | In therapist-guided group, there was an increase in activation of the hippocampus, as well as a decreased connectivity between left IFG and left hippocampus |
|
| SoP | Furmark et al. (2002) | 18 (unmedicated) | PET scan
CBT for eight weeks (each session was 3 hours)
Compared with citalopram-only group | CBT group: decrease in limbic, paralimbic, and PAG hyperactivation. Results maintained at one-year follow-up (multiple brain areas needed to be included to reach statistical significance).
Citalopram group: decrease in thalamic hyperactivation (suggesting decreased sensory input into the amygdala); decrease in vPFC activation |
|
| SP | Paquette et al. (2003) | 12 (unmedicated) | fMRI
4 sessions | Decrease in activation in dlPFC and parahippocampal gyrus |
| Soravia et al. (2016) | 8 (unmedicated) | fMRI
Unspecified number of CBT sessions (though scanning done one month after treatment started) | Anticipation: decreased cerebral blood flow (CBF) in bilateral parahippocampal gyri, ventral anterior thalamus, Brodmann area 8, and the ACC
Postprocessing phase: reduced CBF in the bilateral insula and motor cortex. |
| Straube et al. (2006) | 28 (unclear if medicated) | fMRI
2 sessions (4-5 hours each) | Decrease in activation in ACC and insula |
|
| GAD | Maslowsky et al. (2010) | 7 (unmedicated) | fMRI
8 weeks of CBT
Comparison group was patients on fluoxetine | Increase in activation in vlPFC to angry faces |
| McClure et al. (2007) | 12 (unmedicated) (3 with a diagnosis of social phobia) | fMRI
8 weeks of CBT | Decrease in amygdala activity (not statistically significant) |
| Fonzo et al. (2014) | 21 (unmedicated) | fMRI
10 sessions of CBT | Before treatment, patients showed blunted responses to positive faces in the amygdala, insula, and ACC; they also showed heightened amygdala-insula and amygdala-precuneus connectivity
After treatment: decrease in activation to angry and fearful tasks in the sgACC and amygdala.
Increase in activation to happy tasks in the anterior and posterior insula |
|
| SAD | Doehrmann et al. (2013) | 39 (unmedicated) | fMRI
12 weeks of CBT | Activation changes in areas of lPFC, vPFC, and in the amygdala, none statistically significant |
| Goldin et al. (2013) | 75 (unmedicated) | fMRI
16 sessions of CBT | Cognitive reappraisal of negative self-beliefs was parameter assessed. Amygdala reactivity to negative self-beliefs remained consistent over time
Increase in the dmPFC and dlPFC |
| Goldin et al. (2014) | 59 (unmedicated) | fMRI
16 weeks of CBT | Increase in the superior frontal gyrus, middle occipital lobe, and inferior parietal lobule activity when reacting to social praise
Increases in right superior frontal gyrus and inferior parietal lobule, and decreases in left posterior superior temporal gyrus when reacting to social criticism |
| Klumpp et al. (2013) | 14 (2 on bupropion, the rest unmedicated) | fMRI
12 weeks of CBT | No significant correlation between symptom improvement and activation patterns in dmPFC or mPFC |
| Yuan et al. (2016) | 15 (4 on stable doses of SSRIs) | fMRI
8 weeks of group CBT | Attenuation of dACC-amygdala and dmPFC-amygdala connectivity |
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