A rat model was developed to determine the role of sinus thrombosis an
d elevated sinus pressures in the pathogenesis of dural arteriovenous
malformations (AVMs). Five protocols were tested to compare various si
nus pressures and thrombosis of a sinus: 1) Control I, sham operation
(five animals); 2) Control II, occlusion of the right common carotid a
rtery: the right external jugular vein, and the vein draining the left
transverse sinus, as well as thrombosis of the sagittal sinus (10 ani
mals); 3) arteriovenous fistula (AVF) I, anastomosis of the right comm
on carotid artery to the external jugular vein causing retrograde flow
through the transverse sinus (10 animals); 4) AVF II, anastomosis (as
described in AVF I) and thrombosis of the sagittal sinus (12 animals)
; 5) AVF III, anastomosis (as described in AVF I) as well as thrombosi
s of the sagittal sinus and occlusion of the vein draining the transve
rse sinus on the left (12 animals). Mean arterial and sagittal sinus p
ressures were monitored and cerebral angiograms were obtained intraope
ratively and again 90 days later. Afterward, the animals were sacrific
ed and their brains and dura were examined histologically. Formation o
f a fistula resulted in a significant (p < 0.05) threefold increase in
sagittal sinus pressure in the AVF II group and a significant (p < 0.
05) sixfold increase in the AVF III group. Seven dural AVMs (three in
the AVF II group and four in the AVF III group) were demonstrated angi
ographically and histologically. The seven malformations were located
adjacent to a thrombosed sagittal sinus. All lesions were within the d
ura and sinus wall with direct thrombus-sinus wall connections demonst
rated in four of the malformations. The other three lesions displayed
arteriovenous connections within the sinus wall and dura. These data s
uggest the importance of not only sinus thrombosis but also sinus hype
rtension in the development of a dural AVM.