![]() ![]() Surprisingly, no randomized comparison study of these two methods in GIA treatment have been published. In general endovascular treatment is less invasive and has fewer complications than surgery, and therefore is preferable. There are two treatment modalities that can be offered to patients afflicted with GIA pathology: endovascular or surgical. Therefore, treatment is warranted for most patients suffering from GIAs. The study ISUIA ( Kassell, 1990) proved that the risk of rupture of GIA can reach 40% in five-year follow-up, while treatment of unruptured intracranial aneurysm carries relatively low mortality that does not exceed 2% ( Molyneux, 2005). In contrast, recent papers indicate that rupture of some smaller aneurysms leads to more extensive SAH. Historically GIA rupture is known as devastating due to higher amount of extravasated blood. Therefore, GIA formation can be considered as a “proliferative disease of the vessel wall induced by extravascular activity”. Repeated subadventitial haemorrhages from vasa vasorum are a predominant factor in GIA aneurysm pathogenesis. Krings publication (Krings, 2005) was a breakthrough in large aneurysms formation knowledge he proved that the GIA development in the internal carotid artery (ICA) and vertebral artery (VA) differ from those in other locations. The incidence of intraluminal thrombosis significantly increases with the lumen size of aneurysms in GIAs this phenomena may occur in approximately 60% of cases ( LeRoux, 2003). The histology of GIA wall is different from smaller aneurysms: GIAs often lack a muscular layer as well as elastic laminar layers show degeneration. However, de novo development of GIA has also been described ( Barth, 1994). In flow-related phenomena, constant enlargement of a small aneurysm in the distal part of the neck results in GIA formation. GIA’s and other aneurysms are etiologically divided into “sidewall” and “bifurcation” aneurysms (LeRoux, 2003). The etiology of GIAs is similar to smaller ones ( Lemole, 2000), theories about the development of all saccular aneurysms include congenital and acquired artery defects. If the widest diameter of the aneurysm is equal to or exceeding 25 millimetres (mm), the aneurysm is defined by convention as giant (GIA). Saccular aneurysms are the most common type and account for up to 98% of all intracranial aneurysms ( Yasargil, 1984). There are various intracranial aneurysms: saccular, fusiform, dissecting or mycotic. ![]()
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