- Author: David S Liebeskind, MD; Chief Editor: Helmi L Lutsep, MD more...
A consequence of cerebral aneurysm, aneurysmal subarachnoid hemorrhage (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 has been estimated to be as high as 65%, with most deaths occurring early in the clinical course. See the image below.
Signs and symptoms
Symptoms associated with cerebral aneurysms and SAH are as follows:
Alterations in consciousness
Manifestations of meningeal irritation
Focal neurologic complaints
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 because of differences in aneurysm characteristics. These findings include the following:
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 and distal thromboembolism with prominent focal deficits; these aneurysms may also result in optic atrophy or other cranial neuropathies or cause brainstem compression.
Specific syndromes have been associated with particular aneurysmal locations. For example, aneurysms at the anterior communicating artery, the most common site of aneurysmal SAH (34%), have the following characteristics:
These aneurysms are usually silent until they rupture
Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction.
Neurologic deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%)
See Clinical Presentation for more detail.
Lab studies used in the diagnosis and assessment of cerebral aneurysms include the following:
Complete blood count (CBC) with platelets: Monitor for infection, evaluate anemia, and identify bleeding risk
Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy that increases bleeding risk
Serum chemistries, including electrolytes and osmolarity: Obtain baseline studies to monitor hyponatremia, address arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial pressure
Liver function tests: Identify hepatic dysfunction that may complicate clinical course
Arterial blood gases: Assess blood oxygenation
Imaging studies used in the workup of cerebral aneurysms include the following:
Computed tomography (CT) scanning: Aneurysmal SAH may be detected in 90-95% of cases
Magnetic resonance imaging (MRI): Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scanning with MRI in the detection of SAH is controversial; dolichoectatic and giant aneurysms are identified readily with MRI
Angiography: Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms
Transcranial Doppler ultrasonography: This modality facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the bedside
Single-photon emission CT (SPECT) scanning, positron emission tomography (PET) scanning, xenon-CT (XeCT) scanning: With these techniques, cerebral blood flow studies may depict ischemia associated with vasospasm, although these modalities are not routinely employed
Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with an unwitnessed loss of consciousness
Echocardiography: Cardiac sources of embolism, including endocarditis and myxomas, may be visualized in cases of infectious or neoplastic aneurysms.
Lumbar puncture may help establish the diagnosis of SAH in the absence of focal signs of mass effects. Aneurysmal SAH demonstrates hemorrhagic cerebrospinal fluid with a xanthochromic supernatant, although these findings may be absent within the first few hours following aneurysmal rupture.
See Workup for more detail.
Medical treatment of cerebral aneurysms involves general supportive measures and prevention of complications for individuals who are in the periprocedural period or are poor surgical candidates.
Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel blockers, and prevention of seizures.
Microsurgical techniques focus on exclusion of the aneurysm from the cerebral circulation and reduction of mass effects on adjacent structures. A surgical clip usually is placed across the aneurysm neck with preservation of the parent vessel, eliminating any aneurysmal rests that may subsequently redevelop.
Endovascular coiling of cerebral aneurysms has been found to yield a better clinical outcome than clipping does, with the benefit greatest in patients with a good preoperative grade.[3, 4]
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.
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
Coarctation of the aorta
Other vascular anomalies
Ehlers-Danlos syndrome, type IV
Other collagen type III disorders
Systemic lupus erythematosus
Sickle cell anemia
Neurofibromatosis type 1
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.
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.
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.
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.
In one study of 102 pediatric patients with cerebral aneurysm followed for a mean of 26.8 years, researchers found long-term excess mortality after successful treatment of ruptured aneurysms, especially among males; this excess mortality was largely aneurysm-related.
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.
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.
See the list below:
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.
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|Grade||Clinical Condition at Presentation|
|1||Asymptomatic or minimal headache and slight nuchal rigidity|
|2||Moderately severe or severe headache and nuchal rigidity; cranial neuropathy, no focal deficit|
|3||Drowsiness, confusion, or mild focal deficit|
|4||Stupor, moderate to severe hemiparesis|
|5||Deep coma, decerebrate posturing, moribund appearance|
|Grade||Glasgow Coma Scale Score||Clinical Findings|
|I||15||No headache or focal signs|
|II||15||Headache, nuchal rigidity, no focal signs|
|III||13-14||Headache, nuchal rigidity, no focal signs|
|IV||7-12||Headache, rigidity, focal signs|
|V||3-6||Headache, rigidity, focal signs|
|1||No blood detected|
|2||Diffuse thin layer of subarachnoid blood|
|3||Localized thrombus or thick layer of subarachnoid blood|
|4||Intracerebral or intraventricular hemorrhage with diffuse or no subarachnoid blood|