Evidence mapPaperPMID 41287271Full record

ArticleAnnals of clinical and translational neurology2026

Nationwide Survey of Atopic Myelitis and Plexin D1-Immunoglobulin G-Related Pain.

Jun-Ichi Kira, Xu Zhang, Takayuki Fujii, Mikio Mitsuishi, Miho Ushijima, Sato Yoshidomi, Ayako Sakoda, Tomohiro Imamura, Satoshi Kuwabara, Noriko Isobe and 1 more

Abstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
field-weighted citation impact
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

1 citing paper in PubMed.

  1. Recent advances in autoantibody-mediated pain.Current opinion in supportive and palliative care · 2026
    Review
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

11 authors.

Jun-Ichi KiraTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Xu ZhangTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Takayuki FujiiDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Mikio MitsuishiTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Miho UshijimaTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Sato YoshidomiDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Ayako SakodaTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Tomohiro ImamuraTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.
Satoshi KuwabaraDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Noriko IsobeDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Yuri NakamuraTranslational Neuroscience Research Center, Graduate School of Medicine, International University of Health and Welfare, Okawa, Japan.

Funding

Japan Agency for Medical Research and Development 21ek0109547h0001Japan Agency for Medical Research and Development 22ek0109547h0002Japan Agency for Medical Research and Development 23ek0109547h0003Japan Agency for Medical Research and Development 23ek0109626h0001Japan Agency for Medical Research and Development 23zf0127004h0003Japan Agency for Medical Research and Development 24ek0109626h0002Japan Agency for Medical Research and Development 25ek0109626h0003Japan Agency for Medical Research and Development 25ek0109817h0001Japan Society for the Promotion of Science 22H02985Japan Society for the Promotion of Science 23K18266Japan Society for the Promotion of Science JP21K07464Japan Society for the Promotion of Science JP21K07467Japan Society for the Promotion of Science JP21K15703Japan Society for the Promotion of Science JP22H02985Japan Society for the Promotion of Science JP22K07499Japan Society for the Promotion of Science JP23K06945Japan Society for the Promotion of Science JP23K14761Japan Society for the Promotion of Science JP23K14783Japan Society for the Promotion of Science JP24H00067Japan Society for the Promotion of Science JP24K10666Ministry of Health, Labour and Welfare of Japan 23FC1009
6 · The paper itself

Abstract

objectiveTo elucidate the features of plexin D1-immunoglobulin (Ig)G-associated neuropathic pain and its relationship to atopic myelitis (AM) in a nationwide Japanese survey.

methodsA preliminary survey questionnaire was sent to 1574 selected departments (neurology and pediatrics/pediatric neurology) to explore the numbers of AM and plexin D1-IgG-positive patients between 2018 and 2022. A secondary survey collected detailed patient data via a questionnaire.

resultsIn the preliminary survey, 987 (62.7%) institutions responded, reporting 87 AM patients (49 women) and 11 plexin D1-IgG-positive non-AM patients (8 women). The secondary survey collected 71 AM (plexin D1-IgG-positive: 6/31) and 11 plexin D1-IgG-positive non-AM patients (83.7% recovery rate). In AM, paresthesia/dysesthesia was most frequently experienced (> 90%), followed by pain (> 70%). The underlying diseases in 17 plexin D1-IgG-positive patients, all of whom had neuropathic pain, were AM and small fiber neuropathy in 6 each, neuromyelitis optica spectrum disorder with aquaporin-4-IgG in 2, and painful trigeminal neuropathy, erythromelalgia, and multiple sclerosis in 1 each. When 14 plexin D1-IgG-positive patients (excluding 3 patients with established demyelinating diseases) were compared with 25 plexin D1-IgG-negative AM patients, onset ≥ 50 years old, pain at onset, and allodynia/erythromelalgia/facial pain during the entire disease course were significantly more common in the plexin D1-IgG-positive group. Conversely, atopic disorders and hyperIgEemia were associated with plexin D1-IgG-negative AM but not plexin D1-IgG-positive patients.

interpretationBoth AM and plexin D1-IgG-positive patients present long-standing neuropathic pain, whereas plexin D1-IgG is particularly associated with aged-onset neuropathic pain, allodynia, erythromelalgia, and facial pain, but not atopy.

Indexed as

Immunoglobulin GMyelitisNerve Tissue ProteinsNeuralgiaAdolescentAdultAgedChildFemaleHumansJapanMaleMiddle AgedParesthesiaSurveys and QuestionnairesYoung AdultImmunoglobulin GNerve Tissue Proteinsatopic myelitisautoantibodynationwide surveyneuropathic painplexin D1atopic myelitis

Identifiers

PMID41287271
PMCPMC12968445

What Socratic holds

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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 Socratic graph.