Evidence map›Paper›PMID 34642236›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2021

Autopsy Case of Meningoencephalomyelitis Associated With Glial Fibrillary Acidic Protein Antibody.

Mai Yamakawa, Keenan O Hogan, John Leever, Yasir N Jassam

Open access · goldAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Mai YamakawaFrom the Department of Neurology (M.Y., J.L., Y.N.J.); Department of Pathology and Laboratory Medicine (K.O.H.); Department of Radiology (J.L.), University of Kansas Medical Center; and Hoag Memorial Hospital Presbyterian (Y.N.J.), Pickup Family Neuroscience Institute, Newport Beach, CA.
Keenan O HoganFrom the Department of Neurology (M.Y., J.L., Y.N.J.); Department of Pathology and Laboratory Medicine (K.O.H.); Department of Radiology (J.L.), University of Kansas Medical Center; and Hoag Memorial Hospital Presbyterian (Y.N.J.), Pickup Family Neuroscience Institute, Newport Beach, CA.
John LeeverFrom the Department of Neurology (M.Y., J.L., Y.N.J.); Department of Pathology and Laboratory Medicine (K.O.H.); Department of Radiology (J.L.), University of Kansas Medical Center; and Hoag Memorial Hospital Presbyterian (Y.N.J.), Pickup Family Neuroscience Institute, Newport Beach, CA.
Yasir N JassamFrom the Department of Neurology (M.Y., J.L., Y.N.J.); Department of Pathology and Laboratory Medicine (K.O.H.); Department of Radiology (J.L.), University of Kansas Medical Center; and Hoag Memorial Hospital Presbyterian (Y.N.J.), Pickup Family Neuroscience Institute, Newport Beach, CA. yasir.jassam@hoag.org.
University of Kansas Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesTo describe the autopsy findings and neuropathologic evaluation of autoimmune meningoencephalomyelitis associated with glial fibrillary acidic protein (GFAP) antibody.

methodsWe reviewed the clinical course, imaging, laboratory, and autopsy findings of a patient with autoimmune meningoencephalomyelitis associated with GFAP antibody who had a refractory course to multiple immunosuppressive therapies.

resultsThe patient was a 70-year-old man who was diagnosed as GFAP antibody-associated autoimmune meningoencephalomyelitis. MRI of the head showed linear perivascular enhancement in the midbrain and the basal ganglia. Despite treatment with high-dose corticosteroids, plasma exchange, IV immunoglobulins, and cyclophosphamide, he died with devastating neurologic complications. Autopsy revealed a coexistent neuroendocrine tumor in the small intestine and diffuse inflammation in the brain parenchyma, perivascular spaces, and leptomeninges, with predominant T-cells, macrophages, and activated microglia. B-cells and plasma cells were absent. There was no astrocyte involvement with change in GFAP immunostaining. DISCUSSION: This case illustrates autoimmune meningoencephalomyelitis associated with GFAP antibody in the CSF and coexistent neuroendocrine tumor. The autopsy findings were nonspecific and did not demonstrate astrocyte involvement. Further accumulation of cases is warranted to delineate the utility and pathogenic significance of the GFAP autoantibody.

Indexed as

Autoimmune Diseases of the Nervous SystemMeningoencephalitisNeuroendocrine TumorsAgedAutopsyEncephalomyelitisGlial Fibrillary Acidic ProteinHumansMaleGFAP protein, humanGlial Fibrillary Acidic Protein

Identifiers

PMID34642236
PMCPMC8515200
OpenAlexW3207251897

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.