ArticleFrontiers in immunology2026
CASPR2 antibody-positive glioblastoma-associated pseudoparaneoplastic syndrome: a case report.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paraneoplastic neurological syndromes (PNS) are rare immune-mediated disorders typically associated with systemic malignancies, while their occurrence in primary brain tumors is exceptionally uncommon. We report a 59-year-old man who presented with acute-onset epileptic seizures and transient serum CASPR2 antibody positivity, initially suggestive of autoimmune encephalitis. Early magnetic resonance imaging (MRI) showed T2-FLAIR hyperintensity in the right temporoparietal region without mass effect; however, follow-up imaging revealed a space-occupying lesion consistent with glioblastoma (GBM). The patient experienced transient improvement following immunoglobulin and corticosteroid therapy but achieved definitive recovery only after surgical tumor resection. Histopathology confirmed IDH1 wild-type GBM (CNS WHO Grade IV), and postoperative antibody seroconversion supported a diagnosis of pseudoparaneoplastic syndrome rather than true PNS. This case underscores that primary intracranial tumors such as GBM can transiently mimic autoimmune encephalitis through tumor-associated immune activation without direct antibody pathogenicity. Clinicians should maintain a high index of suspicion for tumor-related processes in patients with neuronal antibody positivity-particularly when antibodies are low-titer, serum-restricted, and clinically discordant-and prioritize dynamic imaging surveillance alongside serial antibody monitoring to avoid diagnostic delay. Further research is warranted to elucidate the mechanisms of GBM-induced immune dysregulation and its implications for neuroimmunological disease.
Indexed as
Identifiers
What OpenQuestion holds
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.