(PS1-65) The Role of Anhedonia Instability in Predicting Treatment Response in Generalized Anxiety Disorder: Findings from an Ecological Momentary Assessment Study

Abstract Text: Anhedonia, a core symptom of depression, also manifests in generalized anxiety disorder (GAD) by impairing positive affect and reward processing (Rizvi et al., 2016). While GAD is defined by permeating, uncontrollable worry across multiple areas of daily life (Rickels & Rynn, 2001), research suggests that anhedonia contributes to its development and persistence. Indeed, Winer et al. (2017) found that anhedonia played a key role in the emergence of anxiety and depressive disorders over time because of the decrease in pleasure exposure and pleasure sensitivity due to avoidance behaviors. Additionally, Grillo (2016) indicated that treating anhedonia has the potential to improve both MDD and GAD due to its status as a shared substrate.
Despite its potential role as a treatment target for both disorders, anhedonia is rarely examined in the context of anxiety-related disorders. Therefore, this study seeks to clarify anhedonia’s predictive value for GAD treatment outcomes. Elucidating this relationship could help enhance patient care and prognosis by emphasizing anhedonia’s transdiagnostic importance in optimizing therapeutic approaches for GAD.
The present study is a reanalysis of Fisher et al. (2019). Data from N=32 individuals who completed personalized modular treatment for mood and anxiety were included. Inclusion criteria were a principal diagnosis of GAD or major depressive disorder (MDD). Participants completed ecological momentary assessment (EMA) for 20 days before receiving a cognitive-behavioral intervention. EMA measures included momentary mood states including anhedonia, anger, fear, positive mood, etc. Pre-EMA baseline depressive and anxious symptoms and post-treatment outcomes were measured via Hamilton Anxiety Rating Scale (HAMA) and Hamilton Rating Scale for Depression (HRSD).
Multiple regression was conducted using R and RStudio to determine whether fluctuations of anhedonia predicted differential treatment outcomes of GAD. Results showed that higher mean squared successive differences (MSSD) of anhedonia significantly predicted less change in anxiety symptoms, as reflected by the HAMA (p = .033). Additionally, higher anhedonia instability also predicted poorer treatment outcomes on the HRSD (p = .042). However, the effect on overall symptom change was not statistically significant. The severity of anhedonic symptoms, represented by the mean score of anhedonia throughout the EMA period, was not a significant predictor of depression or anxiety treatment outcomes.
Findings indicate that ecological fluctuations in anhedonia significantly predict poorer treatment responses for both GAD and MDD symptoms, while average severity does not. Variations in reward sensitivity, indicated by fluctuating anhedonia levels, may impact treatment efficacy more than overall anhedonia severity. These results align with previous findings (Winer et al., 2017) suggesting fluctuating anhedonia reflects inconsistent reward engagement and promotes avoidance behaviors. Addressing reward-deficit processing across disorders may enhance therapeutic approaches and patient outcomes in GAD and MDD.