Background and Purpose The origin and pathogenesis of cerebral aneurys
ms arising at nonbranching sites are not clear. Using our animal model
to induce cerebral aneurysms in rats, we examined induced aneurysms t
hat developed at nonbranching sites. Methods In 35 Sprague-Dawley rats
, the left common carotid artery was ligated and renal hypertension wa
s produced to induce cerebral aneurysms. Twelve months later, the circ
le of Willis was carefully examined under a dissecting microscope. Res
ults Other than cerebral aneurysms at branching sites of the circle of
Willis, aneurysmal bulges developing at nonbranching sites were found
in the proximal portion of the posterior cerebral artery (P1) on the
side of carotid ligation, which supposedly acted as a major collateral
pathway after the ligation, in 19 of 35 treated rats, A total of 30 l
esions were found in these 19 rats, and they were classified into fusi
form aneurysms (22 lesions) involving the entire vessel wall fora shor
t distance and saccular aneurysms (8 lesions) involving only a part of
the wall and expanding laterally from the vessel wall. These P1s beca
me larger in caliber and more tortuous after ligation. Aneurysms devel
oped more frequently in proportion to these changes in these vessels.
Moreover, most aneurysms in these vessels developed at or near the cur
vatures. All of the lateral aneurysms were found on the lateral wall o
f the curvatures of the vessels. Conclusions The present findings indi
cate that cerebral aneurysms at nonbranching sites and saccular aneury
sms at branching sites can occur under the same etiologic conditions.
The site of origin is strongly related to hemodynamic stress.