Evidence map›Paper›PMID 39613748›Full record

ReviewTranslational psychiatry2024

Personalized use of ketamine and esketamine for treatment-resistant depression.

Gustavo C Medeiros, Isabella Demo, Fernando S Goes, Carlos A Zarate, Todd D Gould

Abstract readReview
In one paragraph

Review in Translational psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Treatment-resistant Depression in the Post-ketamine Era: Unmet Needs beyond Rapid Response.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Do sex and gender matter in the pharmacological treatment of depression?Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  11. Article
  12. Review
  13. Korean Medication Algorithm for Depressive Disorder 2025, Fifth Revision: An Executive Summary.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Article
  14. Review
  15. Review
  16. Review
  17. Special Issue: Molecular Research on Depression.International journal of molecular sciences · 2025
    Article
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Gustavo C MedeirosDepartment of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. gustavo.medeiros@som.umaryland.edu.ORCID 0000-0002-0091-1192
Isabella DemoDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Fernando S GoesDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-6262-8264
Carlos A ZarateExperimental Therapeutics & Pathophysiology Branch, Intramural Research Program, NIMH-NIH, Bethesda, MD, USA.
Todd D GouldDepartment of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large and disproportionate portion of the burden associated with major depressive disorder (MDD) is due to treatment-resistant depression (TRD). Intravenous (R,S)-ketamine (ketamine) and intranasal (S)-ketamine (esketamine) are rapid-acting antidepressants that can effectively treat TRD. However, there is variability in response to ketamine/esketamine, and a personalized approach to their use will increase success rates in the treatment of TRD. There is a growing literature on the precision use of ketamine in TRD, and the body of evidence on esketamine is still relatively small. The identification of reliable predictors of response to ketamine/esketamine that are easily translatable to clinical practice is urgently needed. Potential clinical predictors of a robust response to ketamine include a pre-treatment positive family history of alcohol use disorder and a pre-treatment positive history of clinically significant childhood trauma. Pre-treatment versus post-treatment increases in gamma power in frontoparietal brain regions, observed in electroencephalogram (EEG) studies, is a promising brain-based biomarker of response to ketamine, given its time of onset and general applicability. Blood-based biomarkers have shown limited usefulness, with small-effect increases in brain-derived neurotrophic factor (BDNF) being the most consistent indicator of ketamine response. The severity of treatment-emergent dissociative symptoms is typically not associated with a response either to ketamine or esketamine. Future studies should ensure that biomarkers and clinical variables are obtained in a similar manner across studies to allow appropriate comparison across trials and to reduce the signal-to-noise ratio. Most predictors of response to ketamine/esketamine have modest effect sizes; therefore, the use of multivariate predictive models will be needed.

Indexed as

Antidepressive AgentsDepressive Disorder, Treatment-ResistantKetaminePrecision MedicineHumansMajor Depressive DisorderAntidepressive AgentsEsketamineKetamine

Identifiers

PMID39613748
PMCPMC11607365

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.