ArticleCureus2026
Early Non-Contiguous Pachymeningeal Dissemination of Isocitrate Dehydrogenase (IDH)-Wildtype Giant Cell Glioblastoma: A Rare Finding During Adjuvant Therapy.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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5 authors.
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Abstract
Glioblastoma multiforme (GBM) is typically characterized by a locally infiltrative presentation; secondary involvement of the dura mater and leptomeningeal disease are infrequent. A rare diagnostic finding is the isolated "dural tail sign" on contrast-enhanced MRI. While this sign is frequently considered reactive, histopathological findings in highly proliferative instances with increased extracerebral tropism confirm direct neoplastic invasion, justifying intensified surveillance in patients diagnosed with GBM. We present a case of glioblastoma, IDH-wildtype, CNS WHO grade 4, in a patient who exhibited an exceptionally aggressive clinical course. Following maximal safe resection and the standard Stupp protocol, the patient developed multifocal dural and leptomeningeal progression within three months. Radiological findings showed extensive dural thickening and a prominent dural tail sign distinct from the primary site. Histopathological and molecular analyses revealed a highly proliferative giant cell phenotype, aligning with previously documented cases of rapid neuraxis dissemination. These findings, alongside an exceptionally high Ki-67 proliferation index and IDH-wildtype status, underscore a highly aggressive biological profile predisposing the patient to atypical spread. This case highlights the potential for rapid dural dissemination in GBM, occurring within a short interval after diagnosis, surgical treatment, and chemoradiotherapy. The mechanisms underlying this spread are hypothesized to involve neuroglial propagation along pial-arachnoid margins, local seeding secondary to surgical disruption of anatomical planes, and possibly epidural spread associated with a surgical site infection. However, evidence concerning predisposing factors is currently insufficient to modify surgical techniques and perioperative care in known GBM patients. Given the dismal prognosis of leptomeningeal dissemination, early comprehensive molecular profiling and proactive neuraxis imaging are key steps to further characterize tumoral behavior.
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