# Anhedonia and Negative Symptoms in First-Episode Psychosis: A Systematic Review and Meta-Analysis of Prevalence, Mechanisms, and Clinical Implications

**Authors:** Valerio Ricci, Alessandro Sarni, Marialuigia Barresi, Lorenzo Remondino, Giuseppe Maina

PMC · DOI: 10.3390/healthcare13151796 · Healthcare · 2025-07-24

## TL;DR

Anhedonia is a common and persistent negative symptom in first-episode psychosis, affecting up to 53% of patients and significantly impacting their functional outcomes and prognosis.

## Contribution

This study provides a comprehensive meta-analysis of anhedonia prevalence, mechanisms, and treatment outcomes in first-episode psychosis.

## Key findings

- Anhedonia prevalence ranges from 30% to 53% in first-episode psychosis patients.
- Social anhedonia is the strongest predictor of functional outcomes and is linked to increased suicide risk.
- Conventional antipsychotics show limited efficacy for anhedonia, while behavioral activation approaches show promise.

## Abstract

Background: Anhedonia, defined as the diminished capacity to experience pleasure, represents a core negative symptom in first-episode psychosis (FEP) with profound implications for functional outcomes and long-term prognosis. Despite its clinical significance, comprehensive understanding of anhedonia prevalence, underlying mechanisms, and optimal intervention strategies in early psychosis remains limited. Objectives: To systematically examine the prevalence and characteristics of anhedonia in FEP patients, explore neurobiological mechanisms, identify clinical correlates and predictive factors, and evaluate intervention efficacy. Methods: Following PRISMA 2020 guidelines, we conducted comprehensive searches across PubMed, Embase, PsycINFO, and Web of Science databases from January 1990 to June 2025. Studies examining anhedonia and negative symptoms in FEP patients (≤24 months from onset) using validated assessment instruments were included. Quality assessment was performed using appropriate tools for study design. Results: Twenty-one studies comprising 3847 FEP patients met inclusion criteria. Anhedonia prevalence ranged from 30% at 10-year follow-up to 53% during acute phases, demonstrating persistent motivational deficits across illness trajectory. Factor analytic studies consistently supported five-factor negative symptom models with anhedonia as a discrete dimension. Neuroimaging investigations revealed consistent alterations in reward processing circuits, including ventral striatum hypofunction and altered network connectivity patterns. Social anhedonia demonstrated stronger associations with functional outcomes compared to other domains. Epigenetic mechanisms involving oxytocin receptor methylation showed gender-specific associations with anhedonia severity. Conventional antipsychotic treatments showed limited efficacy for anhedonia improvement, while targeted psychosocial interventions demonstrated preliminary promise. Conclusions: Anhedonia showed high prevalence (30–53%) across FEP populations with substantial clinical burden (13-fold increased odds vs. general population). Meta-analysis revealed large effect sizes for anhedonia severity in FEP vs. controls (d = 0.83) and strong negative correlations with functional outcomes (r =·−0.82). Neuroimaging demonstrated consistent ventral striatum dysfunction and altered network connectivity. Social anhedonia emerged as the strongest predictor of functional outcomes, with independent suicide risk associations. Conventional antipsychotics showed limited efficacy, while behavioral activation approaches demonstrated preliminary promise. These findings support anhedonia as a distinct treatment target requiring specialized assessment and intervention protocols in early psychosis care.

## Linked entities

- **Diseases:** psychosis (MONDO:0005485)

## Full-text entities

- **Genes:** OXTR (oxytocin receptor) [NCBI Gene 5021] {aka OT-R, OTR}
- **Diseases:** FEP (MESH:D011618), Negative Symptoms (MESH:D064726), striatum dysfunction (MESH:D020267), Anhedonia (MESH:D059445), motivational deficits (MESH:D009461)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

48 references — full list in the complete paper: https://tomesphere.com/paper/PMC12346823/full.md

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Source: https://tomesphere.com/paper/PMC12346823