Anhedonia is thought to reflect deficits in reward processing that are associated with abnormal activity in mesocorticolimbic brain regions. It is expressed clinically as a deficit in the interest or pleasure in daily activities. More severe
anhedonia in
major depressive disorder (MDD) is a negative predictor of
antidepressant response. It is unknown, however, whether the pathophysiology of
anhedonia represents a viable avenue for identifying
biological markers of
antidepressant treatment response. Therefore, this study aimed to examine the relationships between reward processing and response to
antidepressant treatment using clinical, behavioral, and functional neuroimaging measures. Eighty-seven participants in the first Canadian
Biomarker Integration Network in Depression (CAN-BIND-1) protocol received 8 weeks of open-label
escitalopram. Clinical correlates of reward processing were assessed at baseline using validated scales to measure
anhedonia, and a monetary incentive delay (MID) task during functional neuroimaging was completed at baseline and after 2 weeks of treatment. Response to
escitalopram was associated with significantly lower self-reported deficits in reward processing at baseline. Activity during the reward anticipation, but not the reward consumption, phase of the MID task was correlated with clinical response to
escitalopram at week 8. Early (baseline to week 2) increases in frontostriatal connectivity during reward anticipation significantly correlated with reduction in depressive symptoms after 8 weeks of treatment.
Escitalopram response is associated with clinical and neuroimaging correlates of reward processing. These results represent an important contribution towards identifying and integrating biological, behavioral, and clinical correlates of treatment response. ClinicalTrials.gov: NCT01655706.