Evidence map›Paper›PMID 20113156›Full record

ArticleJournal of neurosurgery2010

Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury.

Roukoz Chamoun, Dima Suki, Shankar P Gopinath, J Clay Goodman, Claudia Robertson

2 registry-linked trialsAbstract read
In one paragraph

Article in Journal of neurosurgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 129 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 6 pooled it
6.2field-weighted citation impact, top 3% 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.

NCT02232347 phase2unknown statusnot on this mapstarted 2014, after this paper: background citation

Effect of Ketamine Versus Sufentanil on Cerebral Glutamate After Traumatic Brain Injury : a Randomized, Double-blinded, Microdialysis Study

TypeinterventionalSponsorPierre-Julien CUNGIRan2014 to 2017Enrolled20ConditionsHead TraumaArmsKetamine, Sufentanil
NCT06337994 phase3completednot on this mapstarted 2024, after this paper: background citation

Treatment of Post-traumatic Cognitive Dysfunction With Memantine Hydrochloride, an N-methyl-D-aspartate (NMDA)-Type Receptor Blocker: a Clinical Trial

TypeinterventionalSponsorAssiut UniversityRan2024 to 2024Enrolled60ConditionsTreatment of Cognitive Deficits After Traumatic Brain InjuryArmsMemantine Hydrochloride
3 · Its place in the literature

Who cites it

129 citing papers in PubMed, 6 syntheses or guidelines pooled it, 244 citations in OpenAlex.

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  7. Nitric oxide and traumatic brain injury.Medical gas research · 2027
    Review
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69 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

5 authors at 2 institutions in 1 country.

Roukoz ChamounDepartment of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.
Dima Suki
Shankar P Gopinath
J Clay Goodman
Claudia Robertson
Baylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · US

Funding

Vascular Mechanisms of Secondary Injury After Traumatic Brain InjuryP01NS038660 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ROBERTSON, CLAUDIA S · 1999 to 2012
$12.1M
NINDS NIH HHS P01 NS038660NINDS NIH HHS P01-NS38660
6 · The paper itself

Abstract

objectAuthors of several studies have implied a key role of glutamate, an excitatory amino acid, in the pathophysiology of traumatic brain injury (TBI). However, the place of glutamate measurement in clinical practice and its impact on the management of TBI has yet to be elucidated. The authors' objective in the present study was to evaluate glutamate levels in TBI, analyzing the factors affecting them and determining their prognostic value.

methodsA prospective study of patients with severe TBI was conducted with an inclusion criterion of a Glasgow Coma Scale score < or = 8 within 48 hours of injury. Invasive monitoring included intracranial pressure measurements, brain tissue PO(2), jugular venous O(2) saturation, and cerebral microdialysis. Patients received standard care including mass evacuation when indicated and treatment of elevated intracranial pressure values. Demographic data, CT findings, and outcome at 6 months of follow-up were recorded.

resultsOne hundred sixty-five patients were included in the study. Initially high glutamate values were predictive of a poor outcome. The mortality rate was 30.3% among patients with glutamate levels > 20 micromol/L, compared with 18% among those with levels < or = 20 micromol/L. Two general patterns were recognized: Pattern 1, glutamate levels tended to normalize over the monitoring period (120 hours); and Pattern 2, glutamate levels tended to increase with time or remain abnormally elevated. Patients showing Pattern 1 had a lower mortality rate (17.1 vs 39.6%) and a better 6-month functional outcome among survivors (41.2 vs 20.7%).

conclusionsGlutamate levels measured by microdialysis appear to have an important role in TBI. Data in this study suggest that glutamate levels are correlated with the mortality rate and 6-month functional outcome.

Indexed as

AdolescentAdultAgedAged, 80 and overBrain InjuriesCerebrumExtracellular SpaceFemaleFollow-Up StudiesGlutamic AcidHumansIntracranial PressureMaleMicrodialysisMiddle AgedOxygenGlutamic AcidOxygen

Identifiers

PMID20113156
PMCPMC3464461
OpenAlexW1880007786

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.