ReviewGenes2026
Intramedullary Spinal Cord Cavernous Angiomas in Familial Cerebral Cavernous Malformations.
Review in Genes, 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
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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.
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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSpinal cord cavernous malformations (SCCMs) are vascular malformations characterized by blood-filled cavities, often leading to neurological deficits. Familial cerebral cavernous malformation (FCCM) is a hereditary condition that predisposes individuals to develop multiple cavernous angiomas. Understanding the incidence, clinical presentation, and management strategies for spinal cavernous angiomas in the context of FCCM is crucial for improving patient outcomes.
methodsThis narrative review synthesizes existing literature on SCCMs in patients with FCCM. A comprehensive search was conducted across multiple databases, including PubMed, Scopus, and Web of Science, utilizing keywords such as "spinal cavernous angiomas" and "familial cerebral cavernomatosis". In addition, a further search was performed among papers discussing FCCM and SCCM, respectively. DISCUSSION: In the paucity of published data about the presence of SCCMs in FCCM, the review highlights the clinical manifestations of SCCMs in both sporadic disease and FCCM, including recurrent hemorrhagic episodes and progressive neurological deficits. Although mutations in the
conclusionsSCCMs in FCCM present distinct challenges in diagnosis and management and their prevalence is probably underestimated. This review underscores the need for heightened awareness among clinicians regarding the hereditary nature of these lesions. Future research should focus on the molecular mechanisms underlying FCCM, aiming to develop targeted therapies and improve clinical outcomes for affected individuals.
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Registered trials
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