Reward activation may not differentiate youths with anxiety from those without

Neural reward circuitry function did not appear to differentiate youths with anxiety from healthy youths, according to results of a randomized clinical trial published in American Journal of Psychiatry.

“Existing work on neural correlates of treatment response in anxious youths is based on the premise of pathological anxiety as a function of altered threat circuitry — primarily amygdala hyperresponsivity,” Stefanie L. Sequeira, MS, of the department of psychology at the University of Pittsburgh, and colleagues wrote. “However, emerging research suggests that aberrant reward circuitry functioning is also implicated in the pathophysiology of anxiety.”

The investigators aimed to evaluate the role baseline functioning in reward circuitry plays in response to psychotherapy among youths with anxiety disorders. Specifically, they compared cognitive behavioral therapy with supportive therapy among this patient population. A total of 72 youths aged 9 to 14 years with anxiety disorders and 37 group-matched healthy comparison youths completed a monetary reward functional MRI task prior to treatment. Sequeira and colleagues categorically defined treatment response at a 35% or higher reduction in diagnostician-rated anxiety severity from pre- to posttreatment assessment. In relation to treatment response, they examined pretreatment neural activation in the striatum and medial prefrontal cortex (mPFC) during monetary wins compared with losses.

Results showed significantly different mPFC activation at baseline to rewards vs. losses among responders, nonresponders and healthy youths. Those with anxiety displayed higher mPFC activity compared with healthy youths; however, this may have been linked to differences in depressive symptoms. The researchers noted planned comparisons between 48 treatment responders and 24 nonresponders showed responders had greater pretreatment neral activation in a cluster that encompassed the subgenual anterior cingulate cortex and nucleus accumbens.

“This work brings us closer to the possibility of improving existing treatments or developing personalized treatments guided by biology,” Sequeira and colleagues wrote. “The study findings, considered with previous research, may signal a need for specific treatments designed for youths low in reward sensitivity. This work also holds promise for understanding the affective neuroscience of anxiety and has potential to inspire conceptual models of the role of reward in the etiology, pathophysiology and course of anxiety.”