Evidence map›Paper›PMID 36107232›Full record

ArticleActa neurochirurgica2022

Quantitative measurement of peritumoral concentrations of glutamate, N-acetyl aspartate, and lactate on magnetic resonance spectroscopy predicts glioblastoma-related refractory epilepsy.

Yawara Nakamura, Akihiro Inoue, Masahiro Nishikawa, Takanori Ohnishi, Hajime Yano, Yonehiro Kanemura, Yoshihiro Ohtsuka, Saya Ozaki, Kosuke Kusakabe, Satoshi Suehiro and 6 more

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Acta neurochirurgica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Optimized Long-TEJournal of magnetic resonance imaging : JMRI · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Elevated glioma-related cortical glutamateBrain communications · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. 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

16 authors at 4 institutions in 1 country.

Yawara NakamuraDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Akihiro InoueDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan. iakihiro3@gmail.com.ORCID http://orcid.org/0000-0002-8951-0263
Masahiro NishikawaDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Takanori OhnishiDepartment of Neurosurgery, Washoukai Sadamoto Hospital, 1-6-1 Takehara, Matsuyama, Ehime, 790-0052, Japan.
Hajime YanoDepartment of Molecular and Cellular Physiology, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Yonehiro KanemuraDepartment of Biomedical Research and Innovation, Institute for Clinical Research, National Hospital Organization Osaka National Hospital, 2-1-14 Hoenzaka, Osaka, 540-0006, Japan.
Yoshihiro OhtsukaDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Saya OzakiDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Kosuke KusakabeDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Satoshi SuehiroDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Daisuke YamashitaDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Seiji ShigekawaDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Hideaki WatanabeDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Riko KitazawaDivision of Diagnostic Pathology, Ehime University Hospital, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Junya TanakaDepartment of Molecular and Cellular Physiology, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Takeharu KuniedaDepartment of Neurosurgery, Ehime University School of Medicine, 454 Shitsukawa, Toon, Ehime, 791-0295, Japan.
Ehime University · JPEhime University Hospital · JPOsaka National Hospital · JPSaiseikai Matsuyama Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreased extracellular glutamate is known to cause epileptic seizures in patients with glioblastoma (GBM). However, predicting whether the seizure will be refractory is difficult. The present study investigated whether evaluation of the levels of various metabolites, including glutamate, can predict the occurrence of refractory seizure in GBM by quantitative measurement of metabolite concentrations on magnetic resonance spectroscopy (MRS).

methodsForty patients were treated according to the same treatment protocol for primary GBM at Ehime University Hospital between April 2017 and July 2021. Of these patients, 23 underwent MRS to determine concentrations of metabolites, including glutamate, N-acetylaspartate, creatine, and lactate, in the tumor periphery by applying LC-Model. The concentration of each metabolite was expressed as a ratio to creatine concentration. Patients were divided into three groups: Type A, patients with no seizures; Type B, patients with seizures that disappeared after treatment; and Type C, patients with seizures that remained unrelieved or appeared after treatment (refractory seizures). Relationships between concentrations of metabolites and seizure types were investigated.

resultsIn 23 GBMs, seizures were confirmed in 11 patients, including Type B in four and Type C in seven. Patients with epilepsy (Type B or C) showed significantly higher glutamate and N-acetylaspartate values than did non-epilepsy patients (Type A) (p < 0.05). No significant differences in glutamate or N-acetylaspartate levels were seen between Types B and C. Conversely, Type C showed significantly higher concentrations of lactate than did Type B (p = 0.001). Cutoff values of lactate-to-creatine, glutamate-to-creatine, and N-acetylaspartate-to-creatine ratios for refractory seizure were > 1.25, > 1.09, and > 0.88, respectively.

conclusionsExtracellular concentrations of glutamate, N-acetylaspartate, and lactate in the tumor periphery were significantly elevated in patients with GBM with refractory seizures. Measurement of these metabolites on MRS may predict refractory epilepsy in such patients and could be an indicator for continuing the use of antiepileptic drugs.

Indexed as

Drug Resistant EpilepsyEpilepsy, Temporal LobeGlioblastomaAspartic AcidCreatineGlutamic AcidHumansLactic AcidMagnetic Resonance SpectroscopyAspartic AcidCreatineGlutamic AcidLactic AcidN-acetylaspartateBrain tumor-related epilepsyGlioblastomaGlutamateLC-ModelMagnetic resonance spectroscopy

Identifiers

PMID36107232
OpenAlexW4295894869

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.