<unk>  means an outpouching of a blood vessel wall that is filled with blood.<unk> s occur at a point of weakness in the vessel wall. This can be because of acquired disease or hereditary factors. The repeated trauma of blood flow against the vessel wall presses against the point of weakness and causes the<unk>  to enlarge. As described by the law of Young-Laplace, the increasing area increases tension against the<unk> al walls, leading to enlargement. In addition, a combination of computational fluid dynamics and morphological indices have been proposed as reliable predictors of cerebral<unk>  rupture. Both high and low wall shear stress of flowing blood can cause<unk>  and rupture. However, the mechanism of action is still unknown. It is speculated that low shear stress causes growth and rupture of large<unk> s through inflammatory response while high shear stress causes growth and rupture of small<unk>  through mural response (response from the blood vessel wall). Other risk factors that contributes to the formation of<unk>  are: cigarette smoking, hypertension, female gender, family history of cerebral<unk> , infection, and trauma. Damage to structural integrity of the arterial wall by shear stress causes an inflammatory response with the recruitment of T cells, macrophages, and mast cells. The inflammatory mediators are: interleukin 1 beta, interleukin 6, tumor necrosis factor alpha (TNF alpha), MMP1, MMP2, MMP9, prostaglandin E2, complement system, reactive oxygen species (ROS), and angiotensin II. However, smooth muscle cells from the tunica media layer of the artery moved into the tunica intima, where the function of the smooth muscle cells changed from contractile function into pro-inflammatory function. This causes the fibrosis of the arterial wall, with reduction of number of smooth muscle cells, abnormal collagen synthesis, resulting in a thinning of the arterial wall and the formation of<unk>  and rupture. No specific gene loci has been identified to be associated with cerebral<unk> s. Generally,<unk> s larger than 7 mm in diameter should be treated because they are prone for rupture. Meanwhile,<unk> s less than 7 mm arise from the anterior and posterior communicating artery and are more easily ruptured when compared to<unk> s arising from other locations. Saccular<unk> s The most common sites of<unk>  saccular<unk> s Saccular<unk> s are almost always the result of hereditary weaknesses in blood vessels and typically occur within the arteries of the circle of Willis, in order of frequency affecting the following arteries: * Anterior communicating artery * Posterior communicating artery * Middle cerebral artery * Internal carotid artery * Tip of basilar artery Saccular<unk> s tend to have a lack of tunica media and elastic lamina around their dilated locations (congenital), with a wall of sac made up of thickened hyalinized intima and adventitia. In addition, some parts of the brain vasculature are inherently weak—particularly areas along the circle of Willis, where small communicating vessels link the main cerebral vessels. These areas are particularly susceptible to saccular<unk> s. Approximately 25% of patients have multiple<unk> s, predominantly when there is a familial pattern.
Intracranial aneurysm
Infectious intracranial aneurysm
Subarachnoid hemorrhage
Cerebral vasculitis
Cerebral atherosclerosis
Cerebral infarction
Intracranial hemorrhage
Carotid artery dissection