Pathogenesis and Radiobiology of Brain Arteriovenous Malformations: Implications for Risk Stratification in Natural History and Post-treatment Course

Achal S. Achrol, B.S.; Raphael Guzman, M.D.; Monika Varga, B.S.; John R. Adler, M.D.; Gary K. Steinberg, M.D.; Ph.D.; Steven D. Chang, M.D.


Neurosurg Focus. 2009;26(5):E9 

In This Article

Pathogenesis of BAVM

The etiology of BAVM remains unknown. Recent studies have suggested a role for genetic factors in the pathogenesis of sporadic BAVM,[1,2,50,73,74,75] which is further supported by reports of familial occurrence of BAVM[97] and the association of BAVM with known systemic genetic disorders (such as Osler-Weber-Rendu disease, Sturge-Weber disease, and Wyburn-Mason syndrome).[19] Molecular characterization of BAVM tissue demonstrates a highly angiogenic milieu with evidence of increased endothelial cell turnover and inflammatory cell-mediated vascular remodeling.[15,16,17,35,36,37,38,39,40] Taken together with a number of reports of de novo BAVM formation,[11,30,78,81,85,92] radiographic growth after initial BAVM diagnosis,[22,23,46,54,55,65,66,68,87] and regrowth after successful treatment of BAVM,[28,29,34,44,48,76] these findings challenge the long-held assumption that BAVMs are static lesions of congenital origin. As such, future studies are needed that explore new paradigms in BAVM pathogenesis, including the possibility that BAVMs might represent benign slowgrowing vascular tumors (not just static congenital lesions), could result from acquired somatic mutations (not just congenital/germline mutations), and may represent aberrant adult vasculogenesis (not just persistent neonatal angiogenesis).


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.