Histopathological changes in brain arteriovenous malformations after embolization using Onyx or N-butyl cyanoacrylate. Laboratory investigation.

Published

Journal Article

OBJECT: The aim of this study was to analyze the histopathological changes in a consecutive series of 32 patients with brain arteriovenous malformations that were resected after undergoing endovascular embolization (22 using Onyx and 10 using N-butyl cyanoacrylate [NBCA]). METHODS: Selections from fixed paraffin-embedded specimens were stained for histological examination with H & E and Verhoeff-van Gieson stain. Lipid dye Oil Red O was used to stain vessel specimens that were embolized using NBCA. Specimens were evaluated for the presence of embolic agent, inflammation, angionecrosis, and evidence of recanalization. These results were correlated with the time interval between the bleeding, embolization, and resection. RESULTS: The smallest vessel occluded by the embolic agent was 5 microm in the Onyx group and 20 microm in the NBCA group. There was evidence of vascular or perivascular inflammation in 20 (90.9%) of 22 and 9 (90%) of 10 specimens after Onyx and NBCA embolization, respectively. Chronic foreign-body giant cells were observed in 12 (54.5%) of 22 specimens after Onyx embolization, but were absent in specimens after NBCA embolization. Angionecrosis of the embolized vessel was observed in 13 (59.1%) of 22 specimens and in 4 (40%) of 10 specimens after Onyx and NBCA embolization, respectively. There was evidence of recanalization in Onyx embolized vessels in 4 (18.2%) of 22 specimens, and there was no evidence of recanalization after NBCA embolization. CONCLUSIONS: Onyx penetrates much smaller vessels than NBCA. Inflammation occurs with both embolic agents at equal frequency. Evidence of chronic foreign-body giant cells and recanalization after Onyx embolization shows a long-standing reaction to Onyx and raises questions about the permanence of occlusion after Onyx embolization.

Full Text

Cited Authors

  • Natarajan, SK; Born, D; Ghodke, B; Britz, GW; Sekhar, LN

Published Date

  • July 2009

Published In

Volume / Issue

  • 111 / 1

Start / End Page

  • 105 - 113

PubMed ID

  • 19326974

Pubmed Central ID

  • 19326974

Electronic International Standard Serial Number (EISSN)

  • 1933-0693

International Standard Serial Number (ISSN)

  • 0022-3085

Digital Object Identifier (DOI)

  • 10.3171/2008.12.jns08441

Language

  • eng