Introduction
Background
Cerebral aneurysms are pathologic focal dilatations of the cerebrovasculature that are prone to rupture. These vascular abnormalities are classified by presumed pathogenesis. Saccular, berry, or congenital aneurysms constitute 90% of all cerebral aneurysms and are located at the major branch points of large arteries. Dolichoectatic, fusiform, or arteriosclerotic aneurysms are elongated outpouchings of proximal arteries that account for 7% of all cerebral aneurysms. Infectious or mycotic aneurysms are situated peripherally and comprise 0.5% of all cerebral aneurysms. Other peripheral lesions include neoplastic aneurysms, rare sequelae of embolized tumor fragments, and traumatic aneurysms. Traumatic injury also may result in dissecting aneurysms in proximal vessels. Microaneurysms of small perforating vessels may result from hypertension.
Saccular aneurysms are situated in the anterior circulation in 85-95% of cases, whereas dolichoectatic aneurysms affect predominantly the vertebrobasilar system. The location of saccular aneurysms at specific arterial segments varies in frequency because of differences in reported study populations. Multiple saccular aneurysms are noted in 20-30% of patients with cerebral aneurysms.
Saccular aneurysms frequently rupture into the subarachnoid space, accounting for 70-80% of spontaneous subarachnoid hemorrhages (SAH). Aneurysmal rupture also may result in intraparenchymal, intraventricular, or subdural hemorrhage. Giant saccular aneurysms, defined as greater than 25 mm in diameter, represent 3-5% of all intracranial aneurysms. Although giant aneurysms may cause SAH, these lesions frequently produce mass effects and result in distal thromboembolism.
Aneurysmal SAH is a catastrophic condition, affecting 30,000 individuals in the United States every year. Most of these individuals (60%) either die or suffer permanent disability; 50% of survivors with favorable outcomes experience considerable neuropsychological dysfunction. Cerebral vasospasm (ie, narrowing of proximal arterial segments) complicates 20-50% of cases and is the major cause of death and disability associated with aneurysmal SAH.
Pathophysiology
The pathogenesis of cerebral aneurysms is related inherently to structural aberrations of the cerebrovasculature, although the etiology of these abnormalities may be diverse. The integrity of the internal elastic lamina is compromised, with associated elastic defects in the adjacent layers of the tunica media and adventitia. Muscular defects of the tunica media and minimal support of adjacent brain parenchyma augment the pathologic potential of chronic hemodynamic stress on the arterial wall. Focal turbulence and discontinuity of the normal architecture at vessel bifurcations may account for the propensity of saccular aneurysm formation at these locations. Distal aneurysms may be smaller compared with proximal sites, yet the risk of rupture may be dissimilar due to the relatively thinner parent artery wall thickness.
The development of cerebral aneurysms remains a controversial topic. A multifactorial etiology is most likely, reflecting the interaction of environmental factors, such as atherosclerosis or hypertension, and a congenital predisposition associated with various vascular abnormalities. Abnormalities of the internal elastic lamina may be congenital or degenerative. Multiple conditions have been associated with cerebral aneurysms; they include the following:
- Autosomal dominant inherited polycystic kidney disease
- Fibromuscular dysplasia
- Arteriovenous malformations
- Osler-Weber-Rendu syndrome
- Coarctation of the aorta
- Other vascular anomalies
- Moyamoya syndrome
- Marfan syndrome
- Ehlers-Danlos syndrome, type IV
- Other collagen type III disorders
- Pseudoxanthoma elasticum
- Alpha1-antitrypsin deficiency
- Systemic lupus erythematosus
- Sickle cell anemia
- Bacterial endocarditis
- Fungal infections
- Neurofibromatosis type 1
- Tuberous sclerosis
Environmental stressors, such as hypertension, have been associated with the presence of multiple aneurysms. A familial inheritance pattern has been noted in fewer than 2% of intracranial aneurysms.
Dolichoectatic aneurysms of proximal vessels most likely have an arteriosclerotic etiology. These tortuous, elongated dilatations devoid of a true aneurysmal neck frequently contain laminated thrombus. Although aneurysmal SAH may occur, these lesions typically exert mass effects on adjacent parenchyma, with brainstem compression and cranial neuropathies, or result in obstruction of cerebrospinal fluid (CSF) outflow or distal thromboembolic sequelae.
Infectious aneurysms typically are situated in distal branches of the middle cerebral artery (MCA; 75-80% of cases), reflecting the embolic origin of these lesions. Cardioembolism of septic material complicates the course of 4% of patients with subacute bacterial endocarditis and may affect other patients with congenital heart disease and right-to-left shunts. Direct extension from lumen to adventitia of septic emboli containing Streptococcus viridans or Staphylococcus aureus (ie, the most common pathogens) may lead to degradation and aneurysm formation. Alternatively, diffuse infiltration from the periphery to the lumen may occur in the setting of meningitis, exemplified by aneurysms of the basal circulation associated with fungal infections. Infectious aneurysms are frequently multiple (20%) and have a greater propensity to bleed than other aneurysms.
Traumatic aneurysms may be located in peripheral cortical branches secondary to contact with the falcine edge or skull fractures associated with penetrating or closed head injury. Traumatic dissecting aneurysms due to expansion of intramural hematomas are noted most commonly at the skull base. These false aneurysms, devoid of all layers of the vessel wall, may compress cranial nerves or lead to distal embolization. Rupture of the internal carotid artery (ICA) may produce a carotid-cavernous fistula.
Distal embolization of tumor fragments from a cardiac myxoma or choriocarcinoma may lead to neoplastic aneurysm formation.
Vein of Galen aneurysms or malformations may cause hydrocephalus associated with aqueductal compromise or congestive heart failure in infants.
Aneurysmal rupture typically results in SAH, with diffuse or focal forms of vasospasm that may lead to ischemia and infarction. Recent animal data suggest therapeutic benefit of nitrite infusions to enhance cerebral perfusion in the setting of aneurysmal SAH. This delayed complication of vasospasm is of unclear pathogenesis but most likely is due to the presence of blood and the formation of multiple substances in the subarachnoid space. Spontaneous thrombosis of an aneurysm and subsequent recurrence have been reported in a few cases.
Frequency
United States
The frequency of cerebral aneurysms is difficult to ascertain because of variation in the definitions of the size of aneurysm and modes of detection. Autopsy series cite prevalences of 0.2-7.9%. Prevalence ranges from 5-10%, with unruptured aneurysms accounting for 50% of all aneurysms. Pediatric aneurysms account for only 2% of all cerebral aneurysms. In the United States, the incidence of ruptured aneurysms is approximately 12 per 100,000 individuals or 30,000 annual cases of aneurysmal SAH. The frequency of cerebral aneurysms has not declined in recent years.
International
Incidence of aneurysmal SAH varies widely depending on geographic location, ranging from 3.9-19.4 per 100,000 individuals, with the highest reported rates in Finland and Japan. Overall, the incidence has been estimated at 10.5 per 100,000 individuals.
Mortality/Morbidity
- Aneurysmal SAH has devastating consequences. About 10% of individuals with aneurysmal SAH die before reaching medical attention, 25% die within 24 hours, and 40-49% die within 3 months. Mortality rate has been estimated to be as high as 65%, with most deaths occurring early in the clinical course.
- Early surgical treatment is associated with higher operative morbidity and mortality rates; however, overall morbidity and mortality rates are lower in patients who undergo surgery. Intraoperative aneurysmal rupture has a combined morbidity and mortality rate of 30-35%.
- Aneurysmal SAH during pregnancy has a mortality rate of 35%, accounting for one of the leading causes of maternal mortality during pregnancy.
Race
The racial predilection of cerebral aneurysms is largely unknown, although a higher incidence has been noted in African Americans, with an odds ratio of 2.1.
Sex
Cerebral aneurysms affect equal numbers of women and men younger than 40 years, although women are affected more frequently in older age groups. Overall, the female-to-male ratio has been estimated at 1.6:1.
- Saccular aneurysms are most common in the anterior communicating artery (ACoA) or anterior cerebral artery (ACA) in men, whereas the junction of the ICA with the posterior communicating artery (PCoA) is the most common site for saccular aneurysms in women.
- Giant aneurysms are 3 times more common in women than men.
- The prognosis of aneurysmal SAH is worse for women than men.
Age
- Cerebral aneurysms are rarely apparent in infants and children. Clinical manifestations increase with age, reaching a peak in people aged 55-60 years.
- Carotid artery is affected most commonly in individuals younger than 18 years.
- The prognosis of aneurysmal SAH worsens with increasing age.
Clinical
History
- The clinical presentation of cerebral aneurysms includes symptoms associated with major aneurysmal rupture (eg, SAH), minor aneurysmal hemorrhage (eg, warning leak or sentinel bleed), nonhemorrhagic manifestations (eg, mass effects or cerebral ischemia), and asymptomatic scenarios (eg, incidental aneurysm detection or identification through screening1 ).
- Although aneurysmal SAH has characteristic historical features, the constellation of symptoms may vary with location, size, shape, and direction of the aneurysm.
- Aneurysmal rupture also may present with intraparenchymal hemorrhage (more common with distal aneurysms), intraventricular hemorrhage (13-28%), or subdural hematoma (2-5%).
- Minor aneurysmal hemorrhage may precede rupture with a wide variation in latency, although these warning leaks also may be clinically silent.
- Giant aneurysms may compress brain parenchyma, resulting in focal neurological complaints.
- Aneurysmal expansion may produce pain or herald new neurological manifestations.
- Traumatic aneurysms may have a delayed presentation, with intracranial hemorrhage or recurrent epistaxis.
- Symptoms associated with cerebral aneurysms and SAH are as follows:
- Headache: This is characterized by the acute onset of severe pain, which patients often describe as "the worst headache of my life." Aneurysmal expansion, thrombosis, or intramural hemorrhage may cause a subacute, unilateral, periorbital headache. Headache does not always accompany aneurysmal SAH.
- Facial pain: Cavernous-carotid aneurysms may produce facial pain.
- Alterations in consciousness: The sudden elevation of intracranial pressure associated with aneurysmal rupture may lead to a precipitous decline in cerebral perfusion pressure, causing syncope (50% of cases). Confusion or mild impairment in alertness also may be noted.
- Seizures: Focal or generalized seizures are present in 25% of aneurysmal SAH cases, with most events occurring within 24 hours of onset.
- Manifestations of meningeal irritation: Neck pain or stiffness, photophobia, sonophobia, or other hyperesthesia may be noted with SAH.
- Autonomic disturbances: Subarachnoid accumulation of products of blood degradation may elicit fever. Nausea or vomiting, sweating, chills, and cardiac arrhythmias also may be present.
- Focal neurological complaints: Hemorrhage or ischemia may manifest with focal deficits including weakness, hemisensory loss, language disturbances, neglect, memory loss, or olfactory disturbances. Focal symptoms are more common with giant aneurysms.
- Visual symptoms: Blurring of vision, diplopia, or visual field defects may be present.
- Respiratory dysfunction or cardiovascular instability: These are ominous signs of brainstem compression.
- Hormonal dysfunction: Intrasellar aneurysms may interfere with pituitary function.
- Epistaxis: This is noted occasionally with traumatic aneurysms.
Physical
- The general examination occasionally reveals manifestations of associated conditions such as subacute bacterial endocarditis, trauma, or collagen-vascular disease.
- Specific physical examination findings may include prominent scalp veins, signs of congestive heart failure (eg, vein of Galen aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).
- Neurologic findings exhibit considerable variability, depending on aneurysm characteristics.
- Aneurysmal SAH may be accompanied by nuchal rigidity, decreased level of consciousness, subhyaloid hemorrhages, pupillary abnormalities (ie, typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits.
- Giant aneurysms or dolichoectatic aneurysms may cause mass effects or distal thromboembolism with prominent focal deficits, optic atrophy or other cranial neuropathies, or brainstem compression.
- Specific syndromes have been associated with particular aneurysmal locations.
- Anterior communicating artery: This is the most common site of aneurysmal SAH (34%). Usually, ACoA aneurysms are silent until they rupture. Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction. Neurological deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%).
- Anterior cerebral artery: Aneurysms of this vessel, excluding ACoA, account for about 5% of all cerebral aneurysms. Most are asymptomatic until they rupture, although frontal lobe syndromes, anosmia, or motor deficits may be noted.
- Middle cerebral artery: Aneurysms of the middle cerebral artery (see Media files 1-2) account for about 20% of aneurysms, typically at first or second division in the sylvian fissure. Aphasia, hemiparesis, hemisensory loss, anosognosia, or visual field defects may be noted.
Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.
Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.
- Posterior communicating artery: Aneurysms present at the junction of the termination of the ICA and PCoA account for 23% of cerebral aneurysms; they are directed laterally, posteriorly, and inferiorly. Pupillary dilatation, ophthalmoplegia, ptosis, mydriasis, and hemiparesis may result.
- Internal carotid artery: Besides PCoA aneurysms, aneurysms of the ICA (see Media file 3) account for about 4% of all cerebral aneurysms. Supraclinoid aneurysms may cause ophthalmoplegia due to compression of cranial nerve (CN) III or variable visual defects and optic atrophy due to compression of the optic nerve. Chiasmal compression may produce bilateral temporal hemianopsia. Hypopituitarism or anosmia may be seen with giant aneurysms. Cavernous-carotid aneurysms exert mass effects within the cavernous sinus, producing ophthalmoplegia and facial sensory loss. Rupture of these aneurysms typically produces a carotid-cavernous fistula, SAH, or epistaxis.
Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.
- Basilar artery: Basilar tip aneurysms (see Media files 4-5) are the most common in the posterior circulation, accounting for 5% of all aneurysms. Clinical findings usually are those associated with SAH, although bitemporal hemianopsia or an oculomotor palsy may occur. Dolichoectatic aneurysms may cause bulbar dysfunction, respiratory difficulties, or neurogenic pulmonary edema.
Cerebral aneurysms. Basilar tip aneurysm illustrated on CT scan (left) and T2-weighted MRI (right).
Cerebral aneurysms. Volume-rendered CT angiography of a basilar tip aneurysm.
- Vertebral artery or posterior inferior cerebellar artery: Aneurysms at these arterial segments typically result in ataxia, bulbar dysfunction, or spinal involvement.
- False localizing signs: False localization may be associated with CN III palsy and hemiparesis in uncal herniation, CN VI palsy with elevated intracranial pressure, homonymous hemianopsia due to posterior cerebral artery compression along the tentorial edge, brainstem dysfunction associated with tonsillar herniation, and vasospasm in remote vessels.
Causes
- Congenital or familial inheritance
- Atherosclerosis
- Hypertension
- Autosomal dominant inherited polycystic kidney disease
- Vasculopathies
- Arteriovenous malformations (see Media file 6)
Cerebral aneurysms. Aneurysm associated with an arteriovenous malformation (AVM) shown on T1-weighted MRI (left), 3D-time-of-flight MRI (middle), and conventional angiography (right).
- Connective tissue disorders
- Sickle cell anemia
- Infections
- Trauma
- Neoplasms
- Cigarette smoking
- Illicit drug use
- Alcohol
More on Cerebral Aneurysms |
 Overview: Cerebral Aneurysms |
| Differential Diagnoses & Workup: Cerebral Aneurysms |
| Treatment & Medication: Cerebral Aneurysms |
| Follow-up: Cerebral Aneurysms |
| Multimedia: Cerebral Aneurysms |
| References |
| Next Page » |
References
Vernooij MW, Ikram MA, Tanghe HL, Vincent AJ, Hofman A, Krestin GP, et al. Incidental findings on brain MRI in the general population. N Engl J Med. Nov 1 2007;357(18):1821-8. [Medline].
Yang CY, Chen YF, Lee CW, Huang A, Shen Y, Wei C, et al. Multiphase CT angiography versus single-phase CT angiography: comparison of image quality and radiation dose. AJNR Am J Neuroradiol. Aug 2008;29(7):1288-95. [Medline].
van Rooij WJ, Sprengers ME, de Gast AN, Peluso JP, Sluzewski M. 3D rotational angiography: the new gold standard in the detection of additional intracranial aneurysms. AJNR Am J Neuroradiol. May 2008;29(5):976-9. [Medline].
Yi AC, Palmer E, Luh GY, Jacobson JP, Smith DC. Endovascular treatment of carotid and vertebral pseudoaneurysms with covered stents. AJNR Am J Neuroradiol. May 2008;29(5):983-7. [Medline].
Yang X, Wu Z, Mu S, Li Y, Lv M. Endovascular treatment of giant and large intracranial aneurysms using the neuroform stent-assisted coil placement. Neurol Res. Jul 2008;30(6):598-602. [Medline].
Tumialán LM, Zhang YJ, Cawley CM, Dion JE, Tong FC, Barrow DL. Intracranial hemorrhage associated with stent-assisted coil embolization of cerebral aneurysms: a cautionary report. J Neurosurg. Jun 2008;108(6):1122-9. [Medline].
Nguyen TN, Raymond J, Guilbert F, Roy D, Bérubé MD, Mahmoud M, et al. Association of endovascular therapy of very small ruptured aneurysms with higher rates of procedure-related rupture. J Neurosurg. Jun 2008;108(6):1088-92. [Medline].
Anzalone N, Scomazzoni F, Cirillo M, Righi C, Simionato F, Cadioli M, et al. Follow-up of coiled cerebral aneurysms at 3T: comparison of 3D time-of-flight MR angiography and contrast-enhanced MR angiography. AJNR Am J Neuroradiol. Sep 2008;29(8):1530-6. [Medline].
Adams WM, Laitt RD, Jackson A. The role of MR angiography in the pretreatment assessment of intracranial aneurysms: a comparative study. AJNR Am J Neuroradiol. Oct 2000;21(9):1618-28. [Medline].
Andaluz N, Zuccarello M. Recent trends in the treatment of cerebral aneurysms: analysis of a nationwide inpatient database. J Neurosurg. Jun 2008;108(6):1163-9. [Medline].
Anson JA, Lawton MT, Spetzler RF. Characteristics and surgical treatment of dolichoectatic and fusiform aneurysms. J Neurosurg. Feb 1996;84(2):185-93. [Medline].
Aoki N, Beck JR, Kitahara T. Reanalysis of unruptured intracranial aneurysm management: effect of a new international study on the threshold probabilities. Med Decis Making. Mar-Apr 2001;21(2):87-96. [Medline].
Becker KJ. Epidemiology and clinical presentation of aneurysmal subarachnoid hemorrhage. Neurosurg Clin N Am. Jul 1998;9(3):435-44. [Medline].
Bederson JB, Awad IA, Wiebers DO. Recommendations for the management of patients with unruptured intracranial aneurysms: A Statement for healthcare professionals from the Stroke Council of the American Heart Association. Stroke. Nov 2000;31(11):2742-50. [Medline].
Benndorf G, Klucznik RP, Meyer D. "Cross-over" technique for horizontal stenting of an internal carotid bifurcation aneurysm using a new self-expandable stent: technical case report. Neurosurgery. Feb 2006;58(1 Suppl):ONS-E172. [Medline].
Brennan JW, Schwartz ML. Unruptured intracranial aneurysms: appraisal of the literature and suggested recommendations for surgery, using evidence-based medicine criteria. Neurosurgery. Dec 2000;47(6):1359-71; discussion 1371-2. [Medline].
Brilstra EH, Rinkel GJ, van der Graaf Y. Treatment of intracranial aneurysms by embolization with coils: a systematic review. Stroke. Feb 1999;30(2):470-6. [Medline].
Broderick JP. Coiling, clipping, or medical management of unruptured intracranial aneurysms: time to randomize?. Ann Neurol. Jul 2000;48(1):5-6. [Medline].
Campi A, Ramzi N, Molyneux AJ, Summers PE, Kerr RS, Sneade M, et al. Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT). Stroke. May 2007;38(5):1538-44. [Medline].
Carter BS, Sheth S, Chang E. Epidemiology of the size distribution of intracranial bifurcation aneurysms: smaller size of distal aneurysms and increasing size of unruptured aneurysms with age. Neurosurgery. Feb 2006;58(2):217-23; discussion 217-23. [Medline].
Chyatte D, Fode NC, Sundt TM. Early versus late intracranial aneurysm surgery in subarachnoid hemorrhage. J Neurosurg. Sep 1988;69(3):326-31. [Medline].
Chyatte D, Porterfield R. Functional outcome after repair of unruptured intracranial aneurysms. J Neurosurg. Mar 2001;94(3):417-21. [Medline].
Connolly ES, Mohr JP, Solomon RA. Unruptured intracranial aneurysms. N Engl J Med. May 6 1999;340(18):1440-1; discussion 1441-2. [Medline].
de Oliveira JG, Beck J, Ulrich C, Rathert J, Raabe A, Seifert V. Comparison between clipping and coiling on the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. Neurosurg Rev. Jan 2007;30(1):22-30; discussion 30-1. [Medline].
Donnan GA, Davis SM. Patients with small, asymptomatic, unruptured intracranial aneurysms and no history of subarachnoid hemorrhage should be treated conservatively. Stroke. Feb 2005;36(2):407. [Medline].
Gonzalez N, Murayama Y, Nien YL. Treatment of unruptured aneurysms with GDCs: clinical experience with 247 aneurysms. AJNR Am J Neuroradiol. Apr 2004;25(4):577-83. [Medline].
Haley EC, Kassell NF, Torner JC. The International Cooperative Study on the Timing of Aneurysm Surgery. The North American experience. Stroke. Feb 1992;23(2):205-14. [Medline].
Hashimoto H, Iida J, Hironaka Y. Use of spiral computerized tomography angiography in patients with subarachnoid hemorrhage in whom subtraction angiography did not reveal cerebral aneurysms. J Neurosurg. Feb 2000;92(2):278-83. [Medline].
Johnston SC, Dowd CF, Higashida RT, Lawton MT, Duckwiler GR, Gress DR. Predictors of rehemorrhage after treatment of ruptured intracranial aneurysms: the Cerebral Aneurysm Rerupture After Treatment (CARAT) study. Stroke. Jan 2008;39(1):120-5. [Medline].
Johnston SC, Wilson CB, Halbach VV. Endovascular and surgical treatment of unruptured cerebral aneurysms: comparison of risks. Ann Neurol. Jul 2000;48(1):11-9. [Medline].
Johnston SC, Zhao S, Dudley RA. Treatment of unruptured cerebral aneurysms in California. Stroke. Mar 2001;32(3):597-605. [Medline].
Juvela S. Recommendations for the management of patients with unruptured intracranial aneurysms. Stroke. Mar 2001;32(3):815-6. [Medline].
Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: a long-term follow-up study. Stroke. Feb 2001;32(2):485-91. [Medline].
Karmonik C, Strother CM, Chen X. Stent-assisted coiling of intracranial aneurysms aided by virtual parent artery reconstruction. AJNR Am J Neuroradiol. Oct 2005;26(9):2368-70. [Medline].
Kim DH, Haney CL, Van Ginhoven G. Utility of outcome measures after treatment for intracranial aneurysms: a prospective trial involving 520 patients. Stroke. Apr 2005;36(4):792-6. [Medline].
Kurre W, Berkefeld J. Materials and techniques for coiling of cerebral aneurysms: how much scientific evidence do we have?. Neuroradiology. Nov 2008;50(11):909-27. [Medline].
Lavine SD, Meyers PM. Application of new techniques and technologies: stenting for cerebral aneurysm. Clin Neurosurg. 2007;54:64-9. [Medline].
Le Roux PD, Winn HR. Management of the ruptured aneurysm. Neurosurg Clin N Am. Jul 1998;9(3):525-40. [Medline].
Lylyk P, Ferrario A, Pasbon B. Buenos Aires experience with the Neuroform self-expanding stent for the treatment of intracranial aneurysms. J Neurosurg. Feb 2005;102(2):235-41. [Medline].
Mayberg MR. Cerebral vasospasm. Neurosurg Clin N Am. Jul 1998;9(3):615-27. [Medline].
McKinney AM, Palmer CS, Truwit CL, Karagulle A, Teksam M. Detection of aneurysms by 64-section multidetector CT angiography in patients acutely suspected of having an intracranial aneurysm and comparison with digital subtraction and 3D rotational angiography. AJNR Am J Neuroradiol. Mar 2008;29(3):594-602. [Medline].
Mitchell P, Kerr R, Mendelow AD, Molyneux A. Could late rebleeding overturn the superiority of cranial aneurysm coil embolization over clip ligation seen in the International Subarachnoid Aneurysm Trial?. J Neurosurg. Mar 2008;108(3):437-42. [Medline].
Molyneux A, Kerr R, Stratton I. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet. Oct 26 2002;360(9342):1267-74. [Medline].
Molyneux AJ, Cekirge S, Saatci I. Cerebral Aneurysm Multicenter European Onyx (CAMEO) trial: results of a prospective observational study in 20 European centers. AJNR Am J Neuroradiol. Jan 2004;25(1):39-51. [Medline].
Molyneux AJ, Kerr RS, Yu LM. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, a. Lancet. Sep 3-9 2005;366(9488):809-17. [Medline].
Niimi Y, Song J, Madrid M. Endosaccular treatment of intracranial aneurysms using matrix coils: early experience and midterm follow-up. Stroke. Apr 2006;37(4):1028-32. [Medline].
Parra A, Kreiter KT, Williams S. Effect of prior statin use on functional outcome and delayed vasospasm after acute aneurysmal subarachnoid hemorrhage: a matched controlled cohort study. Neurosurgery. Mar 2005;56(3):476-84; discussion 476-84. [Medline].
Pierot L, Spelle L, Vitry F. Immediate clinical outcome of patients harboring unruptured intracranial aneurysms treated by endovascular approach: results of the ATENA study. Stroke. Sep 2008;39(9):2497-504. [Medline].
Pluta RM, Dejam A, Grimes G. Nitrite infusions to prevent delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage. JAMA. Mar 23 2005;293(12):1477-84. [Medline].
Qureshi AI, Mohammad Y, Yahia AM. Ischemic events associated with unruptured intracranial aneurysms: multicenter clinical study and review of the literature. Neurosurgery. Feb 2000;46(2):282-9; discussion 289-90. [Medline].
Raaymakers TW, Buys PC, Verbeeten B. MR angiography as a screening tool for intracranial aneurysms: feasibility, test characteristics, and interobserver agreement. AJR Am J Roentgenol. Dec 1999;173(6):1469-75. [Medline].
Reeves BC, Langham J, Lindsay KW, Molyneux AJ, Browne JP, Copley L, et al. Findings of the International Subarachnoid Aneurysm Trial and the National Study of Subarachnoid Haemorrhage in context. Br J Neurosurg. Aug 2007;21(4):318-23; discussion 323-7. [Medline].
Rinkel GJ. Medical management of patients with aneurysmal subarachnoid haemorrhage. Int J Stroke. Aug 2008;3(3):193-204. [Medline].
Rordorf G, Bellon RJ, Budzik RE Jr. Silent thromboembolic events associated with the treatment of unruptured cerebral aneurysms by use of Guglielmi detachable coils: prospective study applying diffusion-weighted imaging. AJNR Am J Neuroradiol. Jan 2001;22(1):5-10. [Medline].
Rosen DS, Macdonald RL. Subarachnoid hemorrhage grading scales: a systematic review. Neurocrit Care. 2005;2(2):110-8. [Medline].
Ryttlefors M, Enblad P, Kerr RS, Molyneux AJ. International subarachnoid aneurysm trial of neurosurgical clipping versus endovascular coiling: subgroup analysis of 278 elderly patients. Stroke. Oct 2008;39(10):2720-6. [Medline].
Salary M, Quigley MR, Wilberger JE Jr. Relation among aneurysm size, amount of subarachnoid blood, and clinical outcome. J Neurosurg. Jul 2007;107(1):13-7. [Medline].
Sanai N, Tarapore P, Lee AC, Lawton MT. The current role of microsurgery for posterior circulation aneurysms: a selective approach in the endovascular era. Neurosurgery. Jun 2008;62(6):1236-49; discussion 1249-53. [Medline].
Schievink WI. Genetics and aneurysm formation. Neurosurg Clin N Am. Jul 1998;9(3):485-95. [Medline].
Schmid-Elsaesser R, Kunz M, Zausinger S, Prueckner S, Briegel J, Steiger HJ. Intravenous magnesium versus nimodipine in the treatment of patients with aneurysmal subarachnoid hemorrhage: a randomized study. Neurosurgery. Jun 2006;58(6):1054-65; discussion 1054-65. [Medline].
Sherlock M, O'sullivan E, Agha A. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf). Mar 2006;64(3):250-4. [Medline].
Sluzewski M, van Rooij WJ. Early rebleeding after coiling of ruptured cerebral aneurysms: incidence, morbidity, and risk factors. AJNR Am J Neuroradiol. Aug 2005;26(7):1739-43. [Medline].
Sluzewski M, van Rooij WJ, Beute GN. Late rebleeding of ruptured intracranial aneurysms treated with detachable coils. AJNR Am J Neuroradiol. Nov-Dec 2005;26(10):2542-9. [Medline].
Solenski NJ, Haley EC, Kassell NF. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med. Jun 1995;23(6):1007-17. [Medline].
Solomon RA, Fink ME, Pile-Spellman J. Surgical management of unruptured intracranial aneurysms. J Neurosurg. Mar 1994;80(3):440-6. [Medline].
Standhardt H, Boecher-Schwarz H, Gruber A, Benesch T, Knosp E, Bavinzski G. Endovascular treatment of unruptured intracranial aneurysms with Guglielmi detachable coils: short- and long-term results of a single-centre series. Stroke. Mar 2008;39(3):899-904. [Medline].
Todd MM, Hindman BJ, Clarke WR. Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med. Jan 13 2005;352(2):135-45. [Medline].
van den Bergh WM, Algra A, van Kooten F. Magnesium sulfate in aneurysmal subarachnoid hemorrhage: a randomized controlled trial. Stroke. May 2005;36(5):1011-5. [Medline].
Velthuis BK, Van Leeuwen MS, Witkamp TD. Computerized tomography angiography in patients with subarachnoid hemorrhage: from aneurysm detection to treatment without conventional angiography. J Neurosurg. Nov 1999;91(5):761-7. [Medline].
Vespa PM, Gobin YP. Endovascular treatment and neurointensive care of ruptured aneurysms. Crit Care Clin. Oct 1999;15(4):667-84. [Medline].
Vinuela F, Murayama Y, Duckwiler GR. Present and future technical developments on aneurysm embolization. Impact on indications and anatomic results. Clin Neurosurg. 2000;47:221-41. [Medline].
Viñuela F, Duckwiler G, Mawad M. Guglielmi detachable coil embolization of acute intracranial aneurysm: perioperative anatomical and clinical outcome in 403 patients. 1997. J Neurosurg. Apr 2008;108(4):832-9. [Medline].
Wermer MJ, van der Schaaf IC, Velthuis BK. Follow-up screening after subarachnoid haemorrhage: frequency and determinants of new aneurysms and enlargement of existing aneurysms. Brain. Oct 2005;128(Pt 10):2421-9. [Medline].
White PM, Wardlaw JM, Easton V. Can noninvasive imaging accurately depict intracranial aneurysms? A systematic review. Radiology. Nov 2000;217(2):361-70. [Medline].
Wiebers DO, Torres VE. Screening for unruptured intracranial aneurysms in autosomal dominant polycystic kidney disease. N Engl J Med. Sep 24 1992;327(13):953-5. [Medline].
Yuki I, Murayama Y, Vinuela F. Development of medical devices for neuro-interventional procedures: special focus on aneurysm treatment. Expert Rev Med Devices. Sep 2005;2(5):539-46. [Medline].
Zada G, Breault J, Liu CY, Khalessi AA, Larsen DW, Teitelbaum GP, et al. Internal carotid artery aneurysms occurring at the origin of fetal variant posterior cerebral arteries: surgical and endovascular experience. Neurosurgery. Jul 2008;63(1 Suppl 1):ONS55-61; discussion ONS61-2. [Medline].
Zaidat OO, Ionita CC, Hussain SI, Alexander MJ, Friedman AH, Graffagnino C. Impact of Ruptured Cerebral Aneurysm Coiling and Clipping on the Incidence of Cerebral Vasospasm and Clinical Outcome. J Neuroimaging. Aug 4 2008;[Medline].
Further Reading
Keywords
intracranial aneurysm, intracerebral aneurysm, saccular aneurysm, berry aneurysm, giant aneurysm, fusiform aneurysm, dolichoectasia, infectious aneurysm, mycotic aneurysm
