Fig. 1.

SDAVFs are localized to dural sleeves of nerve roots. This simplified schematic diagram shows that under pathologic conditions, blood is supplied to a SDAVF lesion by dural arteries (not shown) and then drained in a retrograde manner to normal venous flow through a medullary vein into the coronal venous plexus. Due to the aberrant arteriovenous architecture, the venous system (coronal venous plexus via the medullary vein) receives arterial blood that is “arterialized.” This leads to venous congestion, which can put pressure on the spinal cord to produce clinical symptoms. Although direct evidence is missing, a modified vascular phenotype may be the result of changes in adhesive properties or the expression of specific differentiation-promoting (e.g., FOXO1) or differentiation-inhibiting factors that code for uncoordinated vascular hyperplasia (e.g., VEGFA; PI3K-AKT), vessel diameter malformation, and/or aberrant endothelial cell growth (e.g., MEKK3-KLF2/4). FOXO1, fork-head box O; VEGFA, vascular endothelial growth factor A.