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Ketamine-related neural changes in treatment-resistant depression: A multimodal synthesis of fMRI and PET studies.

Nesreen Sedeek, Carley Rivers, Lucas Williamson, Ayoub Asadi, John G Grundy

Journal of Affective Disorders April 28, 2026 DOI: 10.1016/j.jad.2026.121891 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Systematic review with multimodal synthesis Peer reviewed
Population Adults with treatment-resistant depression
Intervention Ketamine
Topics Ketamine Depression Esketamine
Keywords Brain networks Multimodal synthesis PET Treatment-resistant depression trd FMRI
Key findings Ketamine-related effects were frequently reported in subcortical regions, with distributed and context-dependent effects across cortical systems, and network-level summaries suggested involvement of default-mode, ventral attention, and visual systems.

Abstract

Ketamine produces rapid antidepressant effects in a subset of patients with treatment-resistant depression, yet neuroimaging findings have been difficult to integrate because studies differ in imaging modality, analytic approach, task context, and post-infusion timing. To address this, we conducted a multimodal synthesis of functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) studies of ketamine in adults with treatment-resistant depression, integrating region-level inspection and functional network mapping to evaluate patterns across heterogeneous designs. The findings suggest that ketamine-related effects were frequently reported in subcortical regions, alongside more distributed and context-dependent effects across cortical systems, including prefrontal and anterior cingulate regions. Network-level summaries further suggested involvement of default-mode, ventral attention, and visual systems. Given variability in imaging modality, task state, and scan timing, these results should be interpreted as hypothesis-generating and motivate future harmonized multimodal studies designed to directly link circuit-level changes to molecular mechanisms and clinical response.

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