Author: Kimberly Johnston, Class of 2026

Social anhedonia is a psychological condition characterized by a diminished ability to experience pleasure from social interactions and activities. It is associated with greater symptom severity and poorer response to treatment in individuals with Major Depressive Disorder (MDD). In individuals with MDD and social anhedonia, abnormalities in the orbitofrontal cortex (OFC) may hinder the brain’s ability to properly respond to social rewards. A group of researchers at Stony Brook University conducted the first study relating the structure/function of the OFC with social anhedonia severity in MDD. They hypothesized that (1) social anhedonia would be positively associated with lateral OFC (punishment pathway), and inversely associated with medial OFC (reward pathway) metabolism. And (2) a decrease in lateral OFC metabolism and an increase in medial OFC metabolism are necessary for improving depression severity with treatment. 

Participants in the study were randomly assigned to either receive escitalopram (a medication used to treat depression by increasing levels of serotonin) or a placebo over 8 weeks. Medial/lateral OFC metabolism, thickness, volume, and structural connectivity to the striatum and amygdala were examined. Linear mixed models were used to evaluate the relationships between (1) pretreatment social anhedonia score and pretreatment variables in the medial and lateral regions of the OFC and (2) improvement in depression and percent change in medial and lateral variables. No strong evidence existed to show a significant linear relationship supporting either hypothesis, indicating that the OFC is not the only region involved in social anhedonia and should not be the sole target of treatment. 

In environments such as college where individuals are away from home, initiating social contact requires more effort, heightening the effects of social anhedonia. Future research must investigate the neurobiological mechanisms of social anhedonia to identify therapeutic targets for all disorders in which it is a symptom. Limitations of this study must be addressed to improve generalizability and consider causation as a factor. 

Figure 1: Serotonin, a neurotransmitter.

Works Cited:

[1] Donnely, M., Hsu, D., Gardus J., et al. “Orbitofrontal and striatal metabolism volume, thickness and structural connectivity in relation to social anhedonia in depression: A multimodal study.” Science Direct (2024) https://doi.org/10.1016/j.nicl.2023.103553
[2] Image retrieved from: https://commons.wikimedia.org/wiki/File:Serotonin-2D-skeletal.svg