Researchers at the National Institutes of Health have found overactivation in many brain regions, including the frontal and parietal lobes and the amygdala, in unmedicated children with anxiety disorders.
They also showed that treatment with cognitive behavioral therapy (CBT) led to improvements in clinical symptoms and brain functioning. The findings illuminate the brain mechanisms underlying the acute effects of CBT to treat one of the most common mental disorders. The study, published in the American Journal of Psychiatry, was led by researchers at NIH’s National Institute of Mental Health (NIMH).
Sixty-nine unmedicated children diagnosed with an anxiety disorder underwent 12 weeks of CBT following an established protocol. CBT, which involves changing dysfunctional thoughts and behaviors through gradual exposure to anxiety-provoking stimuli, is the current gold standard for treating anxiety disorders in children.
The researchers used clinician-rated measures to examine the change in children’s anxiety symptoms and clinical functioning from pre- to post-treatment. They also used task-based fMRI to look at whole-brain changes before and after treatment and compare those to brain activity in 62 similarly aged children without anxiety.
Children with anxiety showed greater activity in many brain regions, including cortical areas in the frontal and parietal lobes, which are important for cognitive and regulatory functions, such as attention and emotion regulation. The researchers also observed elevated activity in deeper limbic areas like the amygdala, which are essential for generating strong emotions, such as anxiety and fear.
Following three months of CBT treatment, children with anxiety showed a clinically significant decrease in anxiety symptoms and improved functioning. Increased activation seen before treatment in many frontal and parietal brain regions also improved after CBT, declining to levels equal to or lower than those of non-anxious children. According to the researchers, the reduced activation in these brain areas may reflect more efficient engagement of cognitive control networks following CBT.
However, eight brain regions, including the right amygdala, continued to show higher activity in anxious compared to non-anxious children after treatment. This persistent pattern of enhanced activation suggests some brain regions, particularly limbic areas that modulate responses to anxiety-provoking stimuli, may be less responsive to the acute effects of CBT. Changing activity in these regions may require a longer duration of CBT, additional forms of treatment, or directly targeting subcortical brain areas.
In this study, all children with anxiety received CBT. For comparison purposes, the researchers also measured brain activity in a separate sample of 87 youth who were at high risk for anxiety based on their infant temperament (for example, showing a high sensitivity to new situations). Because these children were not diagnosed with an anxiety disorder, they had not received CBT treatment. Their brain scans were taken at 10 and 13 years.
In adolescents at temperamental risk for anxiety, higher brain activity was related to increased anxiety symptoms over time and matched the brain activity seen in children diagnosed with an anxiety disorder before treatment. This provides preliminary evidence that the brain changes in children with anxiety were driven by CBT and that they may offer a reliable neural marker of anxiety treatment.
