Evidence map›Paper›PMID 30357437›Full record

ArticlePsychopharmacology2018

Effects of ketamine on brain function during response inhibition.

M Steffens, C Neumann, A-M Kasparbauer, B Becker, B Weber, M A Mehta, R Hurlemann, U Ettinger

Abstract readControlled Clinical Trial
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. 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

8 authors at 4 institutions in 3 countries.

M SteffensDepartment of Psychology, University of Bonn, Kaiser-Karl-Ring 9, 53111, Bonn, Germany.
C NeumannDepartment of Anesthesiology, University of Bonn, Bonn, Germany.
A-M KasparbauerDepartment of Psychology, University of Bonn, Kaiser-Karl-Ring 9, 53111, Bonn, Germany.
B BeckerDepartment of Psychiatry and Division of Medical Psychology, University of Bonn, Bonn, Germany.
B WeberCenter for Economics and Neuroscience, University of Bonn, Bonn, Germany.
M A MehtaDepartment of Neuroimaging, Institute of Psychiatry Psychology and Neuroscience, King's College London, London, UK.
R HurlemannDepartment of Psychiatry and Division of Medical Psychology, University of Bonn, Bonn, Germany.
U EttingerDepartment of Psychology, University of Bonn, Kaiser-Karl-Ring 9, 53111, Bonn, Germany. ulrich.ettinger@uni-bonn.de.
University of Bonn · DEKing's College London · GBUniversity Hospital Bonn · DEUniversity of Electronic Science and Technology of China · CN

Funding

Deutsche Forschungsgemeinschaft Et 31/2-1
6 · The paper itself

Abstract

introductionThe uncompetitive N-methyl-D-aspartate (NMDA) receptor (NMDAR) antagonist ketamine has been proposed to model symptoms of psychosis. Inhibitory deficits in the schizophrenia spectrum have been reliably reported using the antisaccade task. Interestingly, although similar antisaccade deficits have been reported following ketamine in non-human primates, ketamine-induced deficits have not been observed in healthy human volunteers.

methodsTo investigate the effects of ketamine on brain function during an antisaccade task, we conducted a double-blind, placebo-controlled, within-subjects study on n = 15 healthy males. We measured the blood oxygen level dependent (BOLD) response and eye movements during a mixed antisaccade/prosaccade task while participants received a subanesthetic dose of intravenous ketamine (target plasma level 100 ng/ml) on one occasion and placebo on the other occasion.

resultsWhile ketamine significantly increased self-ratings of psychosis-like experiences, it did not induce antisaccade or prosaccade performance deficits. At the level of BOLD, we observed an interaction between treatment and task condition in somatosensory cortex, suggesting recruitment of additional neural resources in the antisaccade condition under NMDAR blockage. DISCUSSION: Given the robust evidence of antisaccade deficits in schizophrenia spectrum populations, the current findings suggest that ketamine may not mimic all features of psychosis at the dose used in this study. Our findings underline the importance of a more detailed research to further understand and define effects of NMDAR hypofunction on human brain function and behavior, with a view to applying ketamine administration as a model system of psychosis. Future studies with varying doses will be of importance in this context.

Indexed as

Administration, IntravenousAdultBrainDouble-Blind MethodExcitatory Amino Acid AntagonistsEye MovementsHumansKetamineMalePhotic StimulationReaction TimeReceptors, N-Methyl-D-AspartateSchizophreniaYoung AdultExcitatory Amino Acid AntagonistsKetamineReceptors, N-Methyl-D-AspartateAntisaccadesExperimental model systemEye movementsInhibitory controlKetaminePsychosisSchizophrenia

Identifiers

PMID30357437
OpenAlexW2898382193

What OpenQuestion holds

Textmetadata
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.