Disorder-specific dysfunction in dorsal anterior cingulate cortex and parietal cortex during cognitive reappraisal in anxiety disorder [Letter]

Dear editor Following our recently published article1 in Neuropsychiatric Disease and Treatment, many readers have commented that the effects of comorbid depression cannot be ruled out as a factor in our results, since anxiety disorders and major depression are heterogeneous disorders. We would like to respond to the points made. Impaired cognitive emotion regulation is commonly seen in many psychiatric disorders.2 A recent review concluded that individuals with depressive disorders consistently show decreased activation of the ventrolateral prefrontal cortex (vlPFC) and dorsolateral prefrontal cortex (dlPFC) during cognitive reappraisal.3 Moreover, enhanced activity of the amygdala, which is associated with hyperactive bottom-up emotion responses during downregulation of negative emotion, is a disorder-specific deficit in the recruitment of brain regions during cognitive reappraisal in depression disorder.3 Our meta-analysis was intended to provide a comprehensive description of the brain mechanisms underlying cognitive reappraisal deficits in anxiety disorder. We concluded that patients with anxiety disorder could not recruit the frontoparietal network, including dorsal anterior cingulate cortex (dACC), parietal cortex, dorsomedial prefrontal cortex and supplementary motor area, to down-regulate their emotion responses. Notably, we did not find that abnormalities of vlPFC, dlPFC or amygdala activity were involved in anxiety disorder, which suggests that the cognitive-appraisal-related impairments in emotion regulation that occur in anxiety disorders and major depression have different neural correlates. There are several explanations for our negative findings. First, although we included some patients with anxiety disorder accompanied by depression, they were eligible for inclusion in the meta-analysis as anxiety disorder was the primary diagnosis. Second, although some studies reported that patients with anxiety disorder showed diminished vlPFC and dlPFC activity during downregulation of negative emotion,1 the results are mixed. Our comprehensive meta-analysis was performed to provide a robust description of the neurobiological underpinnings of anxiety. Third, although patients with major depression consistently show enhanced amygdala activity during cognitive reappraisal,3 none of the eight studies included in the meta-analysis reported enhanced amygdala during cognitive reappraisal in anxiety disorders.1 Using a more stringent significance criterion (p