Evidence map›Paper›PMID 36712446›Full record

ArticleFrontiers in neurology2022

Case report: Anti-

Yuki Yokota, Makoto Hara, Natsuki Oshita, Tomotaka Mizoguchi, Haruna Nishimaki, Hiroyuki Hao, Hideto Nakajima

Open access · goldAbstract readCase Reports
In one paragraph

Article in Frontiers in neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 1 institution in 1 country.

Yuki YokotaDivision of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Makoto HaraDivision of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Natsuki OshitaDivision of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Tomotaka MizoguchiDivision of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Haruna NishimakiDivision of Oncologic Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan.
Hiroyuki HaoDivision of Human Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan.
Hideto NakajimaDivision of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: We herein detail our experience with a unique patient with a primary central nervous system (PCNS) B-cell lymphoma concomitant with anti- Case presentation: A 73-year-old Japanese woman presented with acute pyrexia, agitation, and disturbance of consciousness. She gradually developed a reduction in speech frequency and truncal dystonia causing abnormal posture. Brain magnetic resonance imaging (MRI) demonstrated high-intensity lesions in the bilateral frontal lobes, and her cerebrospinal fluid revealed mild pleocytosis. She was diagnosed with acute encephalitis and treated with acyclovir and intravenous dexamethasone; however, no improvement was observed. She was transferred to our hospital 6 weeks after the onset of her symptoms, and anti-NMDAR antibodies were identified in her cerebrospinal fluid through indirect immunolabeling with rat brain frozen sections and cell-based assays with NR1/NR2 transfected HEK cells. Follow-up MRI showed enlargement of the lesions in the right frontal lobe with gadolinium enhancement, suggesting a brain tumor. Stereotactic surgery was implemented, with subsequent pathological examination revealing that the tumor was consistent with diffuse large B-cell lymphoma (DLBCL) without evidence of systemic satellite lesions. Stereotactic irradiative therapies were then added to her treatment regimen, which partly improved her neurological symptoms with only mild cognitive dysfunction still remaining. A decrease in anti-NMDAR antibody titer was also confirmed after immunotherapy and tumor removal. Conclusions: We herein report our experience with a novel case of PCNS-DLBCL masquerading as anti-NMDAR encephalitis that satisfied the diagnostic criteria of "proNMDARE." Treatment, including tumor removal, ameliorated disease severity and antibody titers of the patient. Our findings suggest that anti-NMDAR antibody-associated autoimmunity can be triggered by PCNS B-cell tumors, although primary brain tumors need to be excluded before establishing a diagnosis of autoimmune encephalitis.

Indexed as

anti-NMDAR antibodydiagnostic criteriaencephalitisprimary central nervous system lymphomasyndrome

Identifiers

PMID36712446
PMCPMC9878211
OpenAlexW4315782190

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.