Abnormal spontaneous neural activity in the medial prefrontal cortex and right superior temporal gyrus correlates with anhedonia severity in obsessive-compulsive disorder.

Converging evidence indicated the presence of clinically significant anhedonia in patients with obsessive-compulsive disorder (OCD). Studying anhedonia and its neural correlates in OCD may be beneficial in understanding the pathophysiology and treatment of OCD. However, the neural mechanisms that underlie anhedonia in OCD still remain unclear. The present study was designed to bridge this research gap by using resting-state functional magnetic resonance imaging (fMRI). 29 OCD patients with anhedonia (OCD-AH), 31 OCD patients with normal hedonia (OCD-NH), and 30 healthy controls (HC) received the fMRI scan. The low-frequency fluctuation (ALFF) approach was applied to compare spontaneous neural activity among the three groups. Relationships between the regional ALFFs and anhedonia levels were examined in OCD patients. OCD-AH and OCD-NH manifested overlapping but partially distinct brain alterations. Notably, compared to OCD-NH, the OCD-AH showed decreased ALFF in right superior temporal gyrus (STG) and increased ALFF in medial prefontal cortex (MPFC). Moreover, ALFF values in the right STG were negatively correlated with social anhedonia severity, and ALFFs in the MPFC were positively correlated with both physical and social anhedonia severity in patients with OCD. Relatively small sample size; ALFF could not provide more holistic information of brain network. The present study revealed that abnormal spontaneous neural activity in MPFC is associated with both physical and social anhedonia, while altered intrinsic brain function in right STG is specifically associated with social anhedonia in OCD. These findings contribute to our understandings of the neurobiological mechanisms underlying anhedonia in OCD.

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Copyright © 2019. Published by Elsevier B.V.