An intracranial aneurysm (also called cerebral or brain aneurysm) is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel. Aneurysms in the posterior circulation (basilar artery, vertebral arteries and posterior communicating artery) have a higher risk of rupture. Basilar artery aneurysms represent only 3%-5% of all intracranial aneurysms but are the most common aneurysms in the posterior circulation.

Cerebral aneurysms are classified both by size and shape. Small aneurysms have a diameter of less than 15 mm. Larger aneurysms include those classified as large (15 to 25 mm), giant (25 to 50 mm), and super-giant (over 50 mm). Saccular aneurysms, also known as berry aneurysms, appear as a round outpouching and are the most common form of cerebral aneurysm. Fusiform dolichoectatic aneurysms represent a widening of a segment of an artery around the entire blood vessel, rather than just arising from a side of an artery's wall. They can rupture but usually do not. Microaneurysms, also known as Charcot-Bouchard aneurysms, typically occur in small blood vessels (less than 300 micrometre diameter), most often the lenticulostriate vessels of the basal ganglia, and are associated with chronic hypertension. Charcot–Bouchard aneurysms are a common cause of intracranial hemorrhage. A small, unchanging aneurysm will produce few, if any, symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may be asymptomatic (i.e., experiencing no symptoms at all). Subarachnoid haemorrhage Main article: Subarachnoid hemorrhage § Signs and symptoms If an aneurysm ruptures, blood leaks into the space around the brain. This is called a subarachnoid hemorrhage. Onset is usually sudden with no prodrome, classically presenting as a thunderclap headache worse than previous headaches. Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm. Symptoms of a ruptured aneurysm can include: a sudden severe headache that can last from several hours to days nausea and vomiting drowsiness, confusion and/or loss of consciousness visual abnormalities meningism The risk of a subarachnoid hemorrhage is greater with a saccular aneurysm than a fusiform aneurysm. Microaneurysms A ruptured microaneurysm may cause an intracerebral hemorrhage, presenting as a focal neurological deficit. Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm, or narrowing, of the blood vessels), or multiple aneurysms may also occur. The risk of rupture from a cerebral aneurysm varies according to the size of an aneurysm, with the risk rising as the aneurysm size increases. Risk factors Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Lifestyle diseases including hypertension, smoking, excess alcohol consumption, and obesity are associated with the development of aneurysms.Cocaine use has also been associated with the development of intracranial aneurysms. Other acquired associations with intracranial aneurysms include head trauma and infections. Genetic associations Coarctation of the aorta is also a known risk factor, as is arteriovenous malformation.[8] Genetic conditions associated with connective tissue disease may also be associated with the development of aneurysms. This includes: autosomal dominant polycystic kidney disease, neurofibromatosis type I, Marfan syndrome, multiple endocrine neoplasia type I, pseudoxanthoma elasticum, hereditary hemorrhagic telangiectasia and Ehlers-Danlos syndrome types II and IV. Specific genes have also had reported association with the development of intracranial aneurysms, including perlecan, elastin, collagen type 1 A2, endothelial nitric oxide synthase, endothelin receptor A and cyclin dependent kinase inhibitor. Mutations in interleukin 6 may be protective.[citation needed]. Recently, several genetic loci have been identified as relevant to the development of intracranial aneurysms. These include 1p34-36, 2p14-15, 7q11, 11q25, and 19q13.1-13.3. Pathophysiology Main article: Aneurysm § Pathophysiology Aneurysm means an outpouching of a blood vessel wall that is filled with blood. Aneurysms 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 aneurysm to enlarge. As described by the Law of Young-Laplace, the increasing area increases tension against the aneurysmal walls, leading to enlargement. Saccular aneurysms Saccular aneurysms are almost always the result of hereditary weakness 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 aneurysms tend to have a lack of tunica media and elastic lamina around its dilated location (congenital), with 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 aneurysms. Approximately 25% of patients have multiple aneurysms, predominantly when there is familial pattern. Almost all aneurysms rupture at their apex. This leads to hemorrhage in the subarachnoid space and sometimes in brain parenchyma. Minor leakage from aneurysm may precede rupture, causing warning headaches. About 60% of patients die immediately after rupture. Larger aneurysms have a greater tendency to rupture, though most ruptured aneurysms are less than 10 mm in diameter. Vasospasm, referring to blood vessel constriction, can occur secondary to subarachnoid hemorrhage following a ruptured aneurysm. This is most likely to occur within 21 days and is seen radiologically within 60% of such patients. The vasospasm is thought to be secondary to the apoptosis of inflammatory cells such as macrophages and neutrophils that become trapped in the subarachnoid space. These cells initially invade the subarachnoid space from the circulation in order to phagocytose the hemorrhaged red blood cells. Following apoptosis, it is thought there is a massive degranulation of vasoconstrictors, including endothelins and free radicals, that cause the vasospasm. Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for securing intracranial aneurysms: surgical clipping or endovascular coiling . If possible, either surgical clipping or endovascular coiling is usually performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of rebleeding.

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