Evidence map›Paper›PMID 23540908›Full record

Trial reportBiological psychiatry2013

Neural correlates of rapid antidepressant response to ketamine in treatment-resistant unipolar depression: a preliminary positron emission tomography study.

Paul J Carlson, Nancy Diazgranados, Allison C Nugent, Lobna Ibrahim, David A Luckenbaugh, Nancy Brutsche, Peter Herscovitch, Husseini K Manji, Carlos A Zarate, Wayne C Drevets

Abstract readClinical Trial
In one paragraph

Trial report in Biological psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 6 pooled it
16.8field-weighted citation impact, top 1% of its field
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

84 citing papers in PubMed, 6 syntheses or guidelines pooled it, 163 citations in OpenAlex.

  1. Pooled it
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  7. Trial
  8. Region- and time- specific effects of ketamine on cerebral blood flow: a randomized controlled trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
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  10. Habenula Connectivity and Intravenous Ketamine in Treatment-Resistant Depression.The international journal of neuropsychopharmacology · 2021
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24 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 1 country.

Paul J CarlsonSalt Lake City Veterans Affairs Medical Center and Department of Psychiatry, Salt Lake City, Utah, USA.
Nancy Diazgranados
Allison C Nugent
Lobna Ibrahim
David A Luckenbaugh
Nancy Brutsche
Peter Herscovitch
Husseini K Manji
Carlos A Zarate
Wayne C Drevets
National Institutes of Health · USJohnson & Johnson (United States) · USThe University of Texas Health Science Center at San Antonio · USUniversity of Oklahoma · US

Funding

Glutamatergic Modulators for Rapid & Sustained Antidepressant EffectZIAMH002857 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2009 to 2025
$55.0M
Target validation of novel therapeutic agents in mood disordersZIAMH002927 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2010 to 2025
$37.1M
Intramural NIH HHS ZIA MH002857Intramural NIH HHS ZIA MH002927
6 · The paper itself

Abstract

backgroundMultiple lines of evidence support a role for the glutamatergic system in the pathophysiology of major depressive disorder (MDD). Ketamine, an N-methyl-D-aspartate antagonist, rapidly improves depressive symptoms in individuals with treatment-resistant depression. The neural mechanisms underlying this effect remain unknown.

methodsIn this preliminary study, 20 unmedicated participants with treatment-resistant MDD underwent positron emission tomography to measure regional cerebral glucose metabolism at baseline and following ketamine infusion (single dose of .5mg/kg intravenous over 40minutes). Metabolic data were compared between conditions using a combination of region-of-interest and voxelwise analyses, and differences were correlated with the associated antidepressant response.

resultsWhole-brain metabolism did not change significantly following ketamine. Regional metabolism decreased significantly under ketamine in the habenula, insula, and ventrolateral and dorsolateral prefrontal cortices of the right hemisphere. Metabolism increased postketamine in bilateral occipital, right sensorimotor, left parahippocampal, and left inferior parietal cortices. Improvement in depression ratings correlated directly with change in metabolism in right superior and middle temporal gyri. Conversely, clinical improvement correlated inversely with metabolic changes in right parahippocampal gyrus and temporoparietal cortex.

conclusionsAlthough preliminary, these results indicate that treatment-resistant MDD subjects showed decreased metabolism in the right habenula and the extended medial and orbital prefrontal networks in association with rapid antidepressant response to ketamine. Conversely, metabolism increased in sensory association cortices, conceivably related to the illusory phenomena sometimes experienced with ketamine. Further studies are needed to elucidate how these functional anatomical changes relate to the molecular mechanisms underlying ketamine's rapid antidepressant effects.

Indexed as

BrainBrain MappingPositron-Emission TomographyAdultAntidepressive AgentsDepressive Disorder, Treatment-ResistantFemaleFluorodeoxyglucose F18HumansImage Processing, Computer-AssistedKetamineMagnetic Resonance ImagingMaleMiddle AgedOxygenAntidepressive AgentsFluorodeoxyglucose F18KetamineOxygen

Identifiers

PMID23540908
PMCPMC3672258
OpenAlexW2048046359

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.