Evidence map›Paper›PMID 40018280›Full record

ReviewJournal of neuroendovascular therapy2025

Basic Knowledge and Overview of Brain AVMs.

Michihiro Tanaka

Abstract readReview
In one paragraph

Review in Journal of neuroendovascular therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

1 author.

Michihiro TanakaDepartment of Neurosurgery and Neuroendovascular Surgery, Kameda Medical Center, Kamogawa, Chiba, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain arteriovenous malformations (AVMs) are intricate networks of blood vessels in which arteries connect directly to veins, bypassing the capillary system. This aberration can lead to serious neurological manifestations, including seizures, headaches, and hemorrhagic strokes. The embryonic development of AVMs implicates possible disruptions in arteriovenous differentiation during angiogenesis, improper regression of the primary capillary plexus, or the retention of fetal vasculature as contributing factors. Additionally, genetic mutations and environmental influences during pregnancy may facilitate AVM formation, with identified mutations in genes such as endoglin, activin receptor-like kinase 1, SMAD family member 4, and RAS p21 protein activator 1 disrupting vascular development. Such mutations are associated with conditions like hereditary hemorrhagic telangiectasia and capillary malformation-arteriovenous malformation syndrome, thus highlighting the essential role of genetic counseling in AVM management. This review underscores the importance of a deep comprehension of the embryological and genetic foundations of AVMs to refine diagnostic, therapeutic, and prognostic approaches. The paper advocates for advanced research on intervention strategies and emphasizes the significance of a genetics-focused approach in the clinical management of AVMs.

Indexed as

angiogenesisbrain AVMsembryologyendovascular treatment (EVT)genetics

Identifiers

PMID40018280
PMCPMC11864997

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.