**5. Etiogenesis**

Similar to their pathology, etiogenesis of blister aneurysms remains, despite our best efforts, unclear. Both Stehbens and Ohara have traditionally associated such

lesions with atherosclerosis, a concept that has by now gained wide acceptance [12, 27]. Atheromatous changes affecting the carotid artery lead to degeneration of the internal elastic lamina [28]. The latter is reported to be the major anatomic structure resisting the pressure of blood flow within a given vessel [29]. The end result is an overall weakening and subsequent laceration of the arterial wall (penetrating ulceration) [30]. Focal subadventitial dissection leads to the formulation of a blister aneurysm [14]. For reasons not yet fully understood, this whole process usually takes place at the periphery of an atherosclerotic plaque where its stiff degenerated wall borders that of a normal elastic vessel segment [25]. Further research is needed to explain carotid vulnerability at these locations.

Apart from atherosclerosis, another factor that seems to play an important role in the formation of blister aneurysms is hemodynamics. The anteromedial surface of the supraclinoid carotid segment, where most of blister lesions arise, is curved in such a way that blood flow directly impinges on the arterial wall [4, 11]. In the most probable scenario, increased hemodynamic stress acts on an already diseased, sclerotic arterial segment, and it is the combination of these two that finally results in an aneurysm formation.
