= VENOUS ANGIOMA

= intraparenchymal tangle / cluster of dilated medullary veins converging on a single enlarged draining vein; bleed rarely

• Most common cerebral vascular malformation (~ 60%)!
• Can be considered a normal variant!

Cause: (?) accidents during embryogenesis → occlusion / maldevelopment of superficial / deep veins → creation of compensatory pathway by recruiting and dilating preexisting transmedullary veins

Age: any; M = F

Histo: venous channels without internal elastic lamina, separated by gliotic neural tissue that may calcify; probably representing persistent fetal venous system; normal intervening brain parenchyma

Associated with: blue rubber bleb nevus syndrome with multiple angiomas; increased coexistence of cavernous angiomas which can bleed!

• asymptomatic (common)
• headache, seizure, hemorrhage (unusual)
  Risk of hemorrhage: 0.15% (increased with thrombosed draining vein / coexistent cavernous malformation)

A DVA rarely bleeds and is unlikely the cause of an intraparenchymal hemorrhage → search for a cavernoma, which is best be seen with gradient-echo / blood oxygen level-dependent (BOLD) sequences (= heavily T2* weighted).

• soft + compressible without thrills / pulsations
• distension with Valsalva maneuver

Location: deep cerebral / cerebellar white matter; most commonly adjacent to frontal horn

• “umbrella / spoked-wheel / medusa head” configuration = multiple small radially oriented transmedullary veins at periphery of lesion converging on venous collector
• interspersed normal brain parenchyma
• dense capillary stain in larger lesion
• linear / curvilinear enhancing structure = venous collector draining into superficial dural sinus / deep venous system (ependymal vein)
• NO enlarged arterial vessels

Cx (uncommon): hemorrhage, ischemia

DDx: vascular neoplasm, cavernous vascular malformation, venous varix, Sturge-Weber disease (diffuse pial angiomatosis with venous-type capillaries)