The risk of rupture is less than one percent for aneurysms of this size.The prognosis for a ruptured cerebral aneurysm depends on the extent and location of the aneurysm, the persons age, general health, and neurological condition. Some individuals with a ruptured cerebral aneurysm die from the initial bleeding. Other individuals with cerebral aneurysm recover with little or no neurological deficit. The most significant factors in determining outcome are the Hunt and Hess grade, and age. Generally patients with Hunt and Hess grade I and II hemorrhage on admission to the emergency room and patients who are younger within the typical age range of vulnerability can anticipate a good outcome, without death or permanent disability. Older patients and those with poorer Hunt and Hess grades on admission have a poor prognosis. Generally, about two-thirds of patients have a poor outcome, death, or permanent disability.Increased availability and greater access to medical imaging has caused a rising number of asymptomatic, unruptured cerebral aneurysms to be discovered incidentally during medical imaging investigations. This may lead to surgery including endovascular, or simple monitoring. Recently, an increasing number of aneurysm features have been evaluated in their ability to predict aneurysm rupture status, including aneurysm height, aspect ratio, height-to-width ratio, inflow angle, deviations from ideal spherical or elliptical forms, and radiomics morphological features.
Vasospasm
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. Risk factors
Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Hypertension, smoking, alcoholism, and obesity are associated with the development of brain 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. 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. 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.