SynthesisCNS spectrums2026
Effect of ketamine on reward processing in depressive disorders: a systematic review of neuroimaging studies.
Synthesis in CNS spectrums, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
13 authors.
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Abstract
backgroundAnhedonia and reward-processing deficits are core features of major depressive disorder (MDD) that respond poorly to traditional antidepressants. Ketamine has rapid antidepressant effects, yet its neurofunctional actions within reward circuits remain unclear. We synthesized human neuroimaging evidence on ketamine-related modulation of reward circuitry and implications for anhedonia.
methodsFollowing Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines, we searched Ovid Embase/MEDLINE/PsycINFO, Cochrane Library, Scopus, Web of Science, and Google Scholar. Eligible studies included adults with MDD receiving ketamine or esketamine and undergoing fMRI, PET, or related imaging during rest or reward/emotion tasks. Thirteen studies met inclusion criteria (N = 623; 482 MDD/TRD, 141 controls), mostly randomized, double-blind, and placebo-controlled; no eligible esketamine neuroimaging studies were identified.
resultsIntravenous ketamine (typically 0.5 mg/kg over 40 min) was associated with short-term modulation of fronto-striatal and limbic networks. Resting-state fMRI commonly showed altered ventral striatal-prefrontal/ACC connectivity and broader DMN/salience/executive network reorganization across acute-to-subacute windows (≈2-48 h), with some effects changing at later follow-up (≈10 days). Task-based fMRI showed altered ventral striatal/putaminal responses during reward anticipation/feedback and modulation of medial prefrontal/cingulate activity during emotion processing. PET findings suggested increased prefrontal-cingulate metabolism and region-specific 5-HT₁B binding/availability changes, with baseline ventral striatal 5-HT₁B measures associated with symptom profiles and symptom change.
conclusionsKetamine is associated with rapid reconfiguration of reward-related circuitry, but few studies directly measured anhedonia; findings likely reflect broader reward-processing and antidepressant-associated mechanisms. Larger longitudinal multimodal studies are needed to validate biomarkers and durability.
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