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the internal elastic lamina. The prevalence of intracranial aneurysms has been
estimated at 1%-6% (1-12 million Americans) in large autopsy series. Consid-
erable evidence supports the pathogenesis of aneurysm formation to be related
to genetic predisposition and/or environmental factors, including autosomal
dominant polycystic kidney disease, Marfan's syndrome, Ehler-Danlos type
IV, fibromuscular dysplasia, neurofibromatosis type 1, and age. A common
location of intracranial aneurysms is the arteries at the base of the brain,
known as the Circle of Willis. The rupture of intracranial aneurysms into the
subarachnoid space results in subarachnoid hemorrhage (SAH), a devastat-
ing event with high rates of morbidity (15%-30%) and mortality (30%-67%)
[9-13]. The worldwide incidence of aneurysmal SAH is approximately 1 per
10,000 people with more than 30,000 Americans suffering from SAH in the
United States every year (The American Society of Interventional and Ther-
apeutic Neuroradiology [ASITN]).
Intracranial aneurysms are classified by presumed pathogenesis and geom-
etry. Saccular, berry, or congenital aneurysm represent the majority of all
cerebral aneurysms and are spherical expansions of the vessel wall, typically
occurring at branch points of major intracranial arteries and most often in the
Circle of Willis. The characteristic geometry of a saccular aneurysm is a thin-
walled, balloon-like structure or “dome” communicating with the lumen of a
parent artery at its base through a “neck.” Dolichoectatic, fusiform, or arte-
riosclerotic aneurysms are extended outpouchings of proximal arteries that
account for 7% of all cerebral aneurysms. Infectious or mycotic aneurysms are
situated peripherally and comprise 0.5% of all cerebral aneurysms.
Brain aneurysms may be treated by surgery or by less-invasive endovas-
cular techniques [14]. Clipping across the aneurysmal neck excludes the
aneurysm from the intracranial circulation yielding excellent long-term e-
cacy and protection from aneurysm recurrence or rupture. In the last two
decades, alternative endovascular coil embolization techniques have been
developed to treat intracranial aneurysms. Coil embolization involves the
deployment of tiny platinum coils into the aneurysm through an intravascular
microcatheter reducing intraaneurysmal blood flow and leading to thrombo-
sis of its sac. In both instances, the aim of the procedure is to occlude the
aneurysm with thrombus effectively isolating it from the arterial circulation
and preventing its eventual rupture. Recent endovascular advances with bioac-
tive coils, balloon, and stent-assisted techniques have expanded the range
of intracranial aneurysms that may be treated via coil embolization. Coil
embolization has several advantages over surgical clipping: it produces bet-
ter survival, freedom from disability, and a lower risk of death than surgery
(The International Subarachnoid Aneurysm Trial [ISAT]). Coil embolization,
however, cannot be used in wide-necked irregularly shaped aneurysms due to
diculty achieving adequate filling of the aneurysm sac as well as risk of coil
protrusion into the parent artery [15]. In wide-neck aneurysms, endovascu-
lar stents have been used across the aneurysmal neck in conjunction with coil
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