Originally published by 2 Minute Medicine® (view original article). Reused on AccessMedicine with permission.

1. Cognitive behavioural therapy (CBT) showed reduced activation in specific areas of the brain of adolescents with an anxiety disorder post-treatment.

2. Activation in these areas remained stable in adolescents at risk for AD not receiving CBT, supporting the neural response to cognitive behavioural therapy.

Evidence Rating Level: 1 (Excellent)

Approximately 31.9% of adolescents are affected by anxiety disorders (AD). Cognitive behavioural therapy (CBT) has proven to be an effective treatment for AD and remains the first-line treatment in clinical practice. The neural changes in the brain associated with CBT however have not been studied well.

This randomized control trial investigated the effects of CBT on the brains of adolescents with an AD by having participants complete threat processing tasks (TPT) during fMRI pre and post-CBT treatment. The dot-probe task was used as the TPT. Sixty-nine participants with an AD were compared to a control group of 62 participants without an AD. Additionally, 87 participants at risk for AD were also included to track the stability of neural activation without CBT over time. Participants between the ages of 8-17 with an IQ over 70, proficient in the English language, who had a confirmed diagnosis of an AD (general AD, social AD, separation AD) by semi-structured interview were included. Participants with any serious medical/psychiatric condition, suicidal ideation, substance abuse, or trauma history were excluded. The treatment group received 12 sessions of CBT. Participants were assessed weekly for clinical improvement using the pediatric anxiety scale and the clinical global impressions scale. The primary outcome measured changes to neural activation post-CBT treatment in adolescents with an AD.

Compared to the control group, fMRI data showed comparable or reduced activation in the fronto-parietal regions in the treatment group. Associated regions which included the temporal gyri, the inferior parietal lobules, and the middle occipital gyrus also showed reduced activation. Stability in these areas was seen in the at-risk group supporting treatment response to CBT. No effect was appreciated in the motor cortex, the right amygdala, or the lateral anterior frontal areas. These areas showed hyperactivation pre and post-treatment. A limitation of this study is that a large proportion of participants came from high-income households. It is important to keep in mind that these individuals may have access to resources that complement treatment that their low SES counterparts do not have. This may confound results by overestimating the effects of CBT alone on neural activation. Nevertheless, this study demonstrates important neural changes associated with CBT in specific areas of the brain of adolescents with ADs. Future research may contribute to tailoring CBT to target these areas specifically.

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