Cerebral Aneurysms

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Practice Essentials

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:

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:

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:

See Clinical Presentation for more detail.

Diagnosis

Lab studies used in the diagnosis and assessment of cerebral aneurysms include the following:

Imaging studies used in the workup of cerebral aneurysms include the following:

See Workup for more detail.

Management

Nonsurgical therapy

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.

Surgical treatment

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 treatment

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.[1, 2]

See Treatment and Medication for more detail.

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:

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.

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.[3]

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.

Age

See the list below:

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 screening[4] ).

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:

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.

Specific syndromes have been associated with particular aneurysmal locations.

Causes

See the list below:

Laboratory Studies

Lab studies that may be helpful for diagnosis include the following:

Imaging Studies

Advances in neuroimaging techniques have altered the diagnosis of cerebral aneurysms dramatically. Noninvasive angiographic methods, such as computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), allow for detection and characterization of aneurysms, further enhanced by postprocessing techniques that enable 3-dimensional evaluation of aneurysm morphology. Contemporaneous parenchymal imaging with CT scan or MRI yields a wealth of information that may assist surgical planning. However, minor aneurysmal hemorrhage may not be detected with noninvasive methods.

A study of 20 years of screening results of individuals with a positive family history of SAH found that the yield of long-term screening is substantial even after more than 10 years of follow-up and two initial negative screens. These data suggest that repeated screening should be considered in individuals with 2 or more first-degree relatives who had SAH or unruptured intracranial aneurysms.[5, 6]

CT scan

Aneurysmal SAH may be detected in 90-95% of cases. If CT scan result is negative and SAH is suspected, perform lumbar puncture (LP).

Noncontrast CT scan should be performed, as contrast may obscure detection of SAH.

Curvilinear calcification, aneurysmal thrombosis, or bone erosion may be characterized; however, bone structures also may produce artifacts.

Surrounding edema and an inflammatory reaction may be appreciated with contrast administration following the noncontrast study.

CTA may detect aneurysms greater than 3 mm, providing detailed evaluation of morphology such as relationship to the parent vessel and neck width.

CTA can detect more than 95% of aneurysms identified on conventional angiography. CTA may be superior to MRA because of shorter acquisition times, diminished motion artifacts, and detailed demonstration of other landmarks. However, bone and venous structures may complicate analysis.

Increasing use of CT perfusion in combination with CTA allows for reconstruction of multiphase CT angiographic images, potentially providing greater definition beyond standard CTA.[7]

MRI

Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scan and MRI in detection of SAH is controversial.

MRI may be impractical for patients in unstable condition. Flow voids may be seen extending from the parent vessel into the aneurysm.

Heterogeneous signal intensity adjacent to the aneurysm wall may be seen with thrombus of varying ages, although MRI is relatively insensitive to the presence of calcium.

Dolichoectatic and giant aneurysms are identified readily with MRI. Pulsation artifacts and the presence of turbulence may help to differentiate these aneurysms from other mass lesions, but slow and turbulent flow may preclude visualization on MRA.

MRA may reliably provide 3-dimensional imaging of aneurysms 4 mm or larger.

Phase-contrast techniques may facilitate detection of flow patterns and slow flow. Although phase-contrast MRA is preferable for large aneurysms, 3-dimensional time-of-flight techniques are preferable for small aneurysms. Source images should be inspected routinely in conjunction with the reconstructed views.

Angiography

Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms. Aneurysm location, size, and morphology may be evaluated in the acute or chronic setting with this modality.

Digital subtraction angiography with biplanar magnification views provides details that may be helpful in identifying an acutely ruptured aneurysm.

Aneurysmal irregularity, the presence of a daughter loculus, or focal spasm may be noted with acute rupture. Vasospasm may be depicted reliably and the collateral circulation may be demonstrated.

Perform 4-vessel angiography to identify remote vasospasm and the presence of multiple aneurysms. Acute angiography occasionally yields negative results (eg, due to thrombosis or vasospasm), in which case angiography should be repeated 1-3 weeks later. However, the risk and expense of this procedure may not be appropriate for screening of high-risk individuals.

A junctional dilatation of the terminal carotid artery at the origin of the PCoA may be noted in about 5-10% of patients. These infundibula or conical enlargements of less than 3 mm are unlikely to enlarge or rupture. However, overt aneurysms at the juncture of the terminal carotid artery with a persistent PCoA configuration may be more prone to rupture.

Further refinements in the characterization of cerebral aneurysms are expected following the recent introduction of 3-dimensional rotational angiography. Recent work has demonstrated that this technique may offer superior resolution and increased sensitivity for detection of small aneurysms.[8]

Other imaging studies

Transcranial Doppler ultrasonography: TCD facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the bedside. TCD has exhibited close correlation with angiography in the setting of vasospasm, typically manifesting 3-21 days following aneurysmal SAH.

Single-photon emission computed tomography (SPECT), positron emission tomography (PET), xenon-CT (XeCT): With these techniques, cerebral blood flow studies may depict ischemia associated with vasospasm, although these modalities are not employed routinely.

Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with an unwitnessed loss of consciousness.

Other Tests

Other tests that may be helpful for diagnosis include the following:

Procedures

Lumbar puncture

LP may help to establish the diagnosis of SAH in the absence of focal signs of mass effects. Aneurysmal SAH demonstrates hemorrhagic CSF with a xanthochromic supernatant, although these findings may be absent within the first few hours following aneurysmal rupture.

The opening pressure may be elevated.

WBC count may increase after a delay, reflecting a meningeal inflammatory reaction.

The protein may be elevated with normal or decreased glucose.

Cultures may reveal an infectious etiology.

Ventriculostomy: External drainage of CSF may assist in the management of hydrocephalus and cases with poor clinical grades.

Histologic Findings

Gross pathologic examination may reveal brownish pigmentation and fibrous adhesions of surrounding brain parenchyma. Aneurysm size may be diminished on postmortem examination, although a multilobular shape may be appreciated. A ruptured fundus may be visualized with calcifications of the aneurysm wall and intraluminal thrombus.

Staging

Table 1. Clinical Condition at Presentation



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Table 2. World Federation of Neurological Surgeons Scale



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Table 3. Fisher Grade



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Medical Care

Prehospital care should include assessment of vital signs and neurological status. Airway, breathing, and circulation should be addressed with endotracheal intubation, if necessary, and establishment of intravenous access.

Medical therapy of cerebral aneurysms involves general supportive measures and prevention of complications for individuals who are in the periprocedural period or are poor surgical candidates. Treatment decisions should be based on the clinical status of the patient, vascular anatomy of the aneurysm, and surgical or endovascular considerations.

Medical management of aneurysmal SAH is orchestrated in the ICU, with cardiac monitoring and placement of an arterial line.

Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel blockers, and prevention of seizures.

Following surgical or endovascular aneurysm treatment, blood pressure is maintained at higher levels to diminish complications associated with vasospasm. Vasospasm usually occurs between days 3 and 21, presenting with headache, decreased level of consciousness, and variable neurological deficits. Serial TCD may be employed to detect trends in cerebral blood flow during this period.

Induced hypertension, hypervolemia, and hemodilution (ie, "triple-H therapy") aimed to maintain adequate cerebral perfusion pressure in the setting of impaired cerebrovascular autoregulation. However, guidelines have moved toward maintenance of euvolemia and induced hypertension based on recent literature.[9]

Intraarterial papaverine or endovascular balloon angioplasty may be used to treat vasospasm in select patients.

Infectious aneurysms are friable, with an increased propensity for hemorrhage. Anticoagulation is avoided in this setting. As these lesions resolve with antibiotic therapy, surgical approaches usually are deferred. Regression or evolution of these aneurysms is monitored with serial angiography.

Unruptured Intracranial Aneurysms

The management of unruptured intracranial aneurysms is highly controversial. The International Study of Unruptured Intracranial Aneurysms (ISUIA) indicated a relatively low risk of rupture in small aneurysms without history of SAH. Aneurysms less than 10 mm in size had an annual rupture rate of approximately 0.05%. For posterior communicating, vertebrobasilar/posterior cerebral, or basilar tip aneurysms less than 10 mm, the risk of rupture over 7.5 years approximated 2%, with all other locations harboring a risk of almost 0%. Recent guidelines and an evidence-based systematic review of the literature have formulated recommendations for the care of patients with unruptured intracranial aneurysms, principally based on age, history, and aneurysm size.

The anatomical characterization and morphology of unruptured aneurysms are not readily standardized, however. Some investigators have advocated endovascular or surgical treatment of all aneurysms less than 10 mm if age is less than 50 years, in the absence of contraindications. The presence of cigarette smoking, family history of aneurysms, polycystic kidney disease, or systemic lupus erythematosus may elevate the risk of rupture and should be considered. Asymptomatic aneurysms greater than 10 mm should also be considered for treatment, accounting for age, coexisting medical conditions, and relative risks for treatment.

Considerable surgical mortality and morbidity rates at 1 year (as high as 3.8% and 15.7%, respectively) have been demonstrated in preventive treatment of unruptured aneurysms. The surgeon's experience may be a significant and highly variable factor in operative morbidity rate and functional outcome. More recently, application of diffusion-weighted MRI has demonstrated silent thromboembolic events associated with endovascular treatment of unruptured cerebral aneurysms. Quality-of-life issues, including the psychological morbidity of living with an unruptured intracranial aneurysm, also must be addressed.

Therapeutic decision making must balance endovascular or surgical morbidity and mortality rates with the risk of hemorrhage and other considerations on an individual basis. Future studies in the management of unruptured intracranial aneurysms may systematically account for the evolving technology of advanced endovascular approaches, detailed aneurysm morphology, novel neuroimaging correlates, ethnic and geographical variation, neurocognitive impairment following endovascular or surgical treatment, and quality-of-life issues.

Surgical Therapy

Microsurgical techniques focus on excluding the aneurysm from the cerebral circulation and reducing mass effects on adjacent structures. Various approaches have been developed and tailored to the anatomy and location of the aneurysm. A surgical clip usually is placed across the aneurysm neck with preservation of the parent vessel, eliminating any aneurysmal rests that may redevelop subsequently. Alternative techniques involve proximal or Hunterian ligation, wrapping the aneurysm, and trapping (ie, combined proximal and distal vessel occlusion).

Adjunctive measures have been developed to reduce operative morbidity and to provide cerebral protection. Aneurysmal rupture, the principal surgical complication, may be avoided with induced hypotension, CSF drainage, diuretics, hyperventilation, and use of minimal brain retraction. Hypothermia, with or without circulatory arrest, and systemic hypotension are used commonly. A large study of mild intraoperative hypothermia, however, failed to demonstrate benefit of this adjunctive technique.

Lumbar spinal drainage allows relaxation of brain parenchyma and provides a clean surgical field. Postoperative angiography is performed routinely to check for major vessel occlusion or persistence of an aneurysmal rest. Operative morbidity rate increases with aneurysm size (2.3% for < 5 mm; 6.8% for 6-15 mm, 14% for 16-25 mm) and varies by location.

Optimal timing of aneurysm surgery depends on the clinical status of the patient and associated factors. Early surgery (ie, < 48-96 hours after SAH) is favored for candidates in good condition or those with unstable blood pressure, seizures, mass effect from thrombus, large amounts of blood, or evidence of aneurysm growth or rebleeding. Early surgery carries an increased operative morbidity, although the risks of vasospasm and rebleeding are reduced considerably.

Delayed surgery (ie, 10-14 d after SAH) may be considered for large aneurysms in difficult locations or for candidates in poor clinical condition. Surgery is indicated for ruptured or symptomatic aneurysms in patients without extenuating contraindications or considerably advanced age. Surgery generally is precluded if the clinical status is poor, corresponding to Hunt and Hess grade 4 or 5.

Endovascular Techniques

Advances in endovascular techniques have provided therapeutic alternatives that may be employed even in the setting of acute aneurysmal SAH. These techniques allow parent vessel preservation and may be combined with surgical approaches. Electrolytically detachable platinum coils (eg, Guglielmi detachable coils [GDC]) may be deployed strategically within the aneurysm, promoting thrombosis and eventual obliteration. Wide-neck aneurysms may be more difficult to occlude with these devices. Other materials, such as balloons or glue, also may be used. Complications include vessel perforation, hemorrhage, or distal thromboembolism.

Endovascular therapy or coiling of cerebral aneurysms has proliferated during the past of particular cerebral aneurysms are likely influenced by numerous factors. The International Subarachnoid Aneurysm Trial (ISAT) demonstrated the superiority of coiling with improved clinical outcomes. Seizures were also less common in patients with endovascular treatment, yet late rebleeding was also more common. Selection bias may also have influenced ISAT and, therefore, treatment for a given individual must still be tailored to each case.

A meta-analysis of relevant studies (including ISAT) found that endovascular coiling of cerebral aneurysms yields a better clinical outcome than clipping does, with the benefit greatest in patients with a good preoperative grade.[1, 2] The analysis also confirmed, however, that there is a greater risk of rebleeding with coiling, particularly for patients with a poor preoperative grade. Patient mortality at 1 year with coiling was not significantly different from 1-year mortality with clipping.[1, 2]

Progressive refinement in endovascular techniques and devices tailored for the cerebrovasculature have expanded therapeutic options available for definitive treatment of cerebral aneurysms. More pliable, low-profile stents may be used for stent-assisted coiling for obliteration of wide-necked aneurysms.

Self-expanding or balloon-expandable covered stents may be used for treatment of selected carotid or vertebral artery pseudoaneurysms.[10] The Silk flow-diverter stent allows complete occlusion in most cases after 1 year of treatment, with 7.8% permanent morbidity and 3% mortality.[11]

Large or giant intracranial aneurysms may be treated with a combination of devices, such as stent-assisted coil placement.[12] However, the requirement of dual antiplatelet therapy in stent-assisted coiling may increase the risk of intracranial hemorrhage.[13]

Refinement of endovascular techniques for very small intracranial aneurysms has expanded treatment options, yet complications may also increase in this particular subset.[14]

Although endovascular coiling is a feasible, effective treatment for many elderly patients with ruptured and unruptured intracranial aneurysms, careful patient selection is crucial in view of the risks of the procedure, which may outweigh the risk of rupture in some patients with unruptured aneurysms, according to a systematic review and meta-analysis that included 21 studies of 1511 patients aged 65 years or older.[15, 16]

In this study, long-term occlusion was achieved in 79% of patients.[16] The rate of perioperative stroke (4%) was similar for patients with unruptured and ruptured aneurysms. Intraprocedural rupture occurred in 1% of patients with unruptured aneurysms and in 4% of patients with ruptured aneurysms. Perioperative mortality was 23% for patients with ruptured aneurysms and 1% for those with unruptured aneurysms. At 1-year follow-up, 93% of patients with unruptured aneurysms and 66% of patients with ruptured aneurysms had good outcomes.

Consultations

A multidisciplinary approach to the treatment of cerebral aneurysms is recommended. The following specialists should be a part of the multidisciplinary team:

Diet

Restrict possible surgical candidates to taking nothing by mouth (NPO).

Employ nasogastric feedings for individuals with a decreased level of consciousness.

Recommend a soft, high-fiber diet to alert patients; patients should avoid caffeine.

Activity

Advise bed rest in a quiet dark environment during the initial week following aneurysmal SAH.

Perform passive range of motion exercises and frequent turning.

Assist patients with self-care activities, followed by slow advancement in activity as tolerated.

Medication Summary

Nimodipine has been demonstrated to improve outcome and decrease the incidence of delayed neurological deficits when administered for the first 21 days after aneurysmal SAH. Although the prophylactic role of antiepileptic medications in aneurysmal SAH is controversial, seizures may be treated with these medications. Antihypertensive medications may be needed to control blood pressure. After aneurysmal occlusion, these medications are held typically for 2 weeks. Sedatives and pain control may be needed for aneurysmal SAH. Antiemetics, antacids, and stool softeners also are used routinely.

Nimodipine (Nimotop)

Clinical Context:  For improvement of neurological impairments resulting from spasms following SAH caused by ruptured congenital intracranial aneurysm in patients in good postictal neurological condition.

While studies show benefit in severity of neurological deficits caused by cerebral vasospasm following SAH, no evidence shows that the drug either prevents or relieves spasm of cerebral arteries. Actual mechanism of action unknown but may involve protection of brain against ischemia.

Therapy should start within 96 h of SAH. If capsule cannot be swallowed because patient undergoing surgery or unconscious, a hole can be made at both ends of capsule with 18-gauge needle, and contents extracted into a syringe. Contents then can be emptied into patient's nasogastric tube in situ and washed down tube with 30 mL isotonic saline.

Class Summary

These agents are administered to minimize sequelae of cerebral vasospasm.

Fosphenytoin (Cerebyx)

Clinical Context:  Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.

To avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents (PE). Although can be administered IV and IM, IV is route of choice and should be used in emergency situations.

Concomitant administration of IV benzodiazepine usually necessary to control status epilepticus. Full antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, not immediate.

Class Summary

These agents are administered for treatment and prevention of seizures.

Labetalol (Normodyne, Trandate)

Clinical Context:  Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, thereby decreasing blood pressure.

Hydralazine (Apresoline)

Clinical Context:  Decreases systemic resistance through direct vasodilation of arterioles.

Class Summary

These agents help in controlling systemic blood pressure.

Morphine sulfate (MSIR, Duramorph, Astramorph, MS Contin)

Clinical Context:  Drug of choice for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Various IV doses used; commonly titrated until desired effect obtained.

Class Summary

These agents help in pain relief.

Prochlorperazine (Compazine)

Clinical Context:  May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and depressing reticular activating system. In addition to antiemetic effects, has advantage of augmenting hypoxic ventilatory response, acting as respiratory stimulant at high altitude.

Class Summary

These agents help in minimizing nausea and vomiting.

Ranitidine (Zantac)

Clinical Context:  Inhibits stimulation of H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and hydrogen-ion concentration.

Class Summary

These agents help in relieving gastrointestinal acid reflux.

Docusate sodium (Colace, Dialox, Surfak, Regulax, Sulfalax)

Clinical Context:  For patients who should avoid straining during defecation; allows incorporation of water and fat into stool, causing stool to soften.

Class Summary

These agents help in softening stools and minimizing straining.

Further Outpatient Care

See the list below:

Further Inpatient Care

Following neurosurgical or endovascular intervention, continued care in the ICU generally includes the following:

Inpatient & Outpatient Medications

See the list below:

Transfer

Immediately after prehospital evaluation and emergent stabilization, transfer patients with aneurysmal SAH to a center with neurosurgical expertise.

Deterrence/Prevention

See the list below:

Complications

See the list below:

Prognosis

See the list below:

Patient Education

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What is the mortality rate for aneurysmal subarachnoid hemorrhage (SAH)?What are symptoms of cerebral aneurysms?What are physical findings indicative of cerebral aneurysms?What are neurologic findings suggestive of cerebral aneurysms?What are the characteristics of aneurysmal subarachnoid hemorrhage (SAH)?What is the role of lab studies in the diagnosis and assessment of cerebral aneurysms?What is the role of imaging studies in the diagnosis of cerebral aneurysms?What is included in nonsurgical treatment of cerebral aneurysms?What is the role of surgery in the treatment of cerebral aneurysms?What is the role of endovascular coiling in the treatment of cerebral aneurysms?What are cerebral aneurysms?How are saccular aneurysms characterized?What are aneurysmal subarachnoid hemorrhages (SAH)?What is the pathogenesis of cerebral aneurysms?Which conditions increase the risk for development of cerebral aneurysms?What causes dolichoectatic aneurysms of proximal vessel?What is the 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aneurysms?What are posterior communicating artery (PCoA) aneurysms?What are internal carotid artery (ICA) aneurysms?What are basilar artery aneurysms?What are vertebral artery or posterior inferior cerebellar artery aneurysms?What are false localizing signs of cerebral aneurysms?What are causes of cerebral aneurysms?What are the differential diagnoses for Cerebral Aneurysms?What is the role of lab studies in the diagnosis of cerebral aneurysms?What is the role of imaging studies in the workup of cerebral aneurysms?What is the role of CT scanning in the workup of cerebral aneurysms?What is the role of MRI in the workup of cerebral aneurysms?What is the role of angiography in the workup of cerebral aneurysms?Which imaging studies may be helpful in the workup of cerebral aneurysms?Which cardiac tests may be helpful in the workup of cerebral aneurysms?What is the role of lumbar puncture (LP) in the workup of cerebral aneurysms?Which histologic findings are characteristic of cerebral aneurysms?How are cerebral aneurysms staged?What is included in prehospital care for cerebral aneurysms?What are the medical treatment options for cerebral aneurysms?What conditions must be managed prior to definitive treatment for cerebral aneurysms?What care is needed following surgical or endovascular cerebral aneurysm treatment?What is the role of triple-H therapy in the treatment of cerebral aneurysms?What is the role of intraarterial papaverine or endovascular balloon angioplasty in the treatment of cerebral aneurysms?How are infectious cerebral aneurysms managed?What are treatment guidelines for unruptured intracranial aneurysms?What are the treatment options for unruptured intracranial aneurysms?What is the role of surgery in the treatment of unruptured intracranial aneurysms?What is the basis of treatment selection for unruptured intracranial aneurysms?What are the surgical approaches to the treatment of cerebral aneurysms?What measures are used to reduce operative morbidity in the treatment of cerebral aneurysms?What is the role of lumbar spinal drainage the treatment of cerebral aneurysms?What is the optimal timing of surgery for cerebral aneurysms?When is surgical delay indicated for the treatment of cerebral aneurysms?What is the role of endovascular techniques in the treatment of cerebral aneurysms?What is the efficacy of endovascular therapy for cerebral aneurysms?What are the advantages of low-profile stents in the treatment of cerebral aneurysms?What are the indications for self-expanding covered stents in the treatment of cerebral aneurysms?Which endovascular techniques are used for treatment of large or giant intracranial cerebral aneurysms?What are considerations regarding endovascular coiling for the treatment of cerebral aneurysms in elderly patients?Which specialists should be included on a multidisciplinary treatment team for cerebral aneurysms?Which dietary modifications are used in the treatment of cerebral aneurysms?Which activity restrictions are used in the treatment of cerebral aneurysms?Which medications are used in the management of cerebral aneurysms?Which medications in the drug class Stool softeners are used in the treatment of Cerebral Aneurysms?Which medications in the drug class Antacids are used in the treatment of Cerebral Aneurysms?Which medications in the drug class Antiemetics are used in the treatment of Cerebral Aneurysms?Which medications in the drug class Analgesics are used in the treatment of Cerebral Aneurysms?Which medications in the drug class Antihypertensives are used in the treatment of Cerebral Aneurysms?Which medications in the drug class Antiepileptics are used in the treatment of Cerebral Aneurysms?Which medications in the drug class Calcium channel blockers are used in the treatment of Cerebral Aneurysms?What is included in outpatient care following treatment for cerebral aneurysms?What is included in ICU care of cerebral aneurysms?Which medications are used in the treatment of cerebral aneurysms?What are the indications for transfer of patients with cerebral aneurysms?How are is neurological injury prevented in cerebral aneurysms?What are possible complications of cerebral aneurysms?What is the prognosis of cerebral aneurysms?What is included in patient education for cerebral aneurysms?

Author

David S Liebeskind, MD, FAAN, FAHA, FANA, Professor of Neurology and Director, Neurovascular Imaging Research Core, Director, Vascular Neurology Residency Program, Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine; Director, UCLA Outpatient Stroke and Neurovascular Programs; Director, UCLA Cerebral Blood Flow Laboratory; Associate Neurology Director, UCLA Stroke Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Consultant, Abbott Vascular, Inc. .

Additional Contributors

Draga Jichici, MD, FRCP, FAHA, Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Disclosure: Nothing to disclose.

References

  1. Brooks M. Does Coiling Beat Clipping for Ruptured Aneurysms? Medscape Medical News. Dec 31 2012. Available at http://www.medscape.com/viewarticle/776939. Accessed: Jan 16, 2013.
  2. Li H, Pan R, Wang H, Rong X, Yin Z, Milgrom DP, et al. Clipping versus coiling for ruptured intracranial aneurysms: a systematic review and meta-analysis. Stroke. 2013 Jan. 44(1):29-37. [View Abstract]
  3. Koroknay-Pál P, Laakso A, Lehto H, Seppä K, Kivisaari R, Hernesniemi J, et al. Long-term Excess Mortality in Pediatric Patients With Cerebral Aneurysms. Stroke. 2012 Aug. 43(8):2091-6. [View Abstract]
  4. 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. 2007 Nov 1. 357(18):1821-8. [View Abstract]
  5. Brooks M. Serial Screening for Cerebral Aneurysm Fruitful. Medscape Medical News. Available at http://www.medscape.com/viewarticle/824618. Accessed: May 14, 2014.
  6. Bor AS, Rinkel GJ, van Norden J, Wermer MJ. Long-term, serial screening for intracranial aneurysms in individuals with a family history of aneurysmal subarachnoid haemorrhage: a cohort study. Lancet Neurol. 2014 Apr. 13(4):385-92. [View Abstract]
  7. 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. 2008 Aug. 29(7):1288-95. [View Abstract]
  8. 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. 2008 May. 29(5):976-9. [View Abstract]
  9. [Guideline] Connolly ES Jr, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012 Jun. 43 (6):1711-37. [View Abstract]
  10. Yi AC, Palmer E, Luh GY, Jacobson JP, Smith DC. Endovascular treatment of carotid and vertebral pseudoaneurysms with covered stents. AJNR Am J Neuroradiol. 2008 May. 29(5):983-7. [View Abstract]
  11. Berge J, Biondi A, Machi P, Brunel H, Pierot L, Gabrillargues J, et al. Flow-Diverter Silk Stent for the Treatment of Intracranial Aneurysms: 1-year Follow-Up in a Multicenter Study. AJNR Am J Neuroradiol. 2012 Feb 2. [View Abstract]
  12. 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. 2008 Jul. 30(6):598-602. [View Abstract]
  13. 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. 2008 Jun. 108(6):1122-9. [View Abstract]
  14. 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. 2008 Jun. 108(6):1088-92. [View Abstract]
  15. Harding A. Careful selection key to coiling in elderly aneurysm patients. Medscape Medical News. May 23, 2013.
  16. Sturiale CL, Brinjikji W, Murad MH, Lanzino G. Endovascular Treatment of Intracranial Aneurysms in Elderly Patients: A Systematic Review and Meta-Analysis. Stroke. 2013 May 16. [View Abstract]
  17. 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. 2008 Sep. 29(8):1530-6. [View Abstract]
  18. 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. 2000 Oct. 21(9):1618-28. [View Abstract]
  19. Alg VS, Sofat R, Houlden H, Werring DJ. Genetic risk factors for intracranial aneurysms: A meta-analysis in more than 116,000 individuals. Neurology. 2013 Jun 4. 80(23):2154-65. [View Abstract]
  20. Andaluz N, Zuccarello M. Recent trends in the treatment of cerebral aneurysms: analysis of a nationwide inpatient database. J Neurosurg. 2008 Jun. 108(6):1163-9. [View Abstract]
  21. Anson JA, Lawton MT, Spetzler RF. Characteristics and surgical treatment of dolichoectatic and fusiform aneurysms. J Neurosurg. 1996 Feb. 84(2):185-93. [View Abstract]
  22. 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. 2001 Mar-Apr. 21(2):87-96. [View Abstract]
  23. Becker KJ. Epidemiology and clinical presentation of aneurysmal subarachnoid hemorrhage. Neurosurg Clin N Am. 1998 Jul. 9(3):435-44. [View Abstract]
  24. 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. 2000 Nov. 31(11):2742-50. [View Abstract]
  25. 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. 2006 Feb. 58(1 Suppl):ONS-E172. [View Abstract]
  26. Brennan JW, Schwartz ML. Unruptured intracranial aneurysms: appraisal of the literature and suggested recommendations for surgery, using evidence-based medicine criteria. Neurosurgery. 2000 Dec. 47(6):1359-71; discussion 1371-2. [View Abstract]
  27. Brilstra EH, Rinkel GJ, van der Graaf Y. Treatment of intracranial aneurysms by embolization with coils: a systematic review. Stroke. 1999 Feb. 30(2):470-6. [View Abstract]
  28. Broderick JP. Coiling, clipping, or medical management of unruptured intracranial aneurysms: time to randomize?. Ann Neurol. 2000 Jul. 48(1):5-6. [View Abstract]
  29. 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. 2007 May. 38(5):1538-44. [View Abstract]
  30. 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. 2006 Feb. 58(2):217-23; discussion 217-23. [View Abstract]
  31. Chyatte D, Fode NC, Sundt TM. Early versus late intracranial aneurysm surgery in subarachnoid hemorrhage. J Neurosurg. 1988 Sep. 69(3):326-31. [View Abstract]
  32. Chyatte D, Porterfield R. Functional outcome after repair of unruptured intracranial aneurysms. J Neurosurg. 2001 Mar. 94(3):417-21. [View Abstract]
  33. Connolly ES, Mohr JP, Solomon RA. Unruptured intracranial aneurysms. N Engl J Med. 1999 May 6. 340(18):1440-1; discussion 1441-2. [View Abstract]
  34. 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. 2007 Jan. 30(1):22-30; discussion 30-1. [View Abstract]
  35. Donnan GA, Davis SM. Patients with small, asymptomatic, unruptured intracranial aneurysms and no history of subarachnoid hemorrhage should be treated conservatively. Stroke. 2005 Feb. 36(2):407. [View Abstract]
  36. Gonzalez N, Murayama Y, Nien YL. Treatment of unruptured aneurysms with GDCs: clinical experience with 247 aneurysms. AJNR Am J Neuroradiol. 2004 Apr. 25(4):577-83. [View Abstract]
  37. Haley EC, Kassell NF, Torner JC. The International Cooperative Study on the Timing of Aneurysm Surgery. The North American experience. Stroke. 1992 Feb. 23(2):205-14. [View Abstract]
  38. 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. 2000 Feb. 92(2):278-83. [View Abstract]
  39. 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. 2008 Jan. 39(1):120-5. [View Abstract]
  40. Johnston SC, Wilson CB, Halbach VV. Endovascular and surgical treatment of unruptured cerebral aneurysms: comparison of risks. Ann Neurol. 2000 Jul. 48(1):11-9. [View Abstract]
  41. Johnston SC, Zhao S, Dudley RA. Treatment of unruptured cerebral aneurysms in California. Stroke. 2001 Mar. 32(3):597-605. [View Abstract]
  42. Juvela S. Recommendations for the management of patients with unruptured intracranial aneurysms. Stroke. 2001 Mar. 32(3):815-6. [View Abstract]
  43. Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: a long-term follow-up study. Stroke. 2001 Feb. 32(2):485-91. [View Abstract]
  44. Karmonik C, Strother CM, Chen X. Stent-assisted coiling of intracranial aneurysms aided by virtual parent artery reconstruction. AJNR Am J Neuroradiol. 2005 Oct. 26(9):2368-70. [View Abstract]
  45. Kim DH, Haney CL, Van Ginhoven G. Utility of outcome measures after treatment for intracranial aneurysms: a prospective trial involving 520 patients. Stroke. 2005 Apr. 36(4):792-6. [View Abstract]
  46. Kurre W, Berkefeld J. Materials and techniques for coiling of cerebral aneurysms: how much scientific evidence do we have?. Neuroradiology. 2008 Nov. 50(11):909-27. [View Abstract]
  47. Lavine SD, Meyers PM. Application of new techniques and technologies: stenting for cerebral aneurysm. Clin Neurosurg. 2007. 54:64-9. [View Abstract]
  48. Le Roux PD, Winn HR. Management of the ruptured aneurysm. Neurosurg Clin N Am. 1998 Jul. 9(3):525-40. [View Abstract]
  49. Lylyk P, Ferrario A, Pasbon B. Buenos Aires experience with the Neuroform self-expanding stent for the treatment of intracranial aneurysms. J Neurosurg. 2005 Feb. 102(2):235-41. [View Abstract]
  50. Mayberg MR. Cerebral vasospasm. Neurosurg Clin N Am. 1998 Jul. 9(3):615-27. [View Abstract]
  51. 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. 2008 Mar. 29(3):594-602. [View Abstract]
  52. 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. 2008 Mar. 108(3):437-42. [View Abstract]
  53. 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. 2002 Oct 26. 360(9342):1267-74. [View Abstract]
  54. 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. 2004 Jan. 25(1):39-51. [View Abstract]
  55. 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. 2005 Sep 3-9. 366(9488):809-17. [View Abstract]
  56. Niimi Y, Song J, Madrid M. Endosaccular treatment of intracranial aneurysms using matrix coils: early experience and midterm follow-up. Stroke. 2006 Apr. 37(4):1028-32. [View Abstract]
  57. 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. 2005 Mar. 56(3):476-84; discussion 476-84. [View Abstract]
  58. 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. 2008 Sep. 39(9):2497-504. [View Abstract]
  59. Pluta RM, Dejam A, Grimes G. Nitrite infusions to prevent delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage. JAMA. 2005 Mar 23. 293(12):1477-84. [View Abstract]
  60. Qureshi AI, Mohammad Y, Yahia AM. Ischemic events associated with unruptured intracranial aneurysms: multicenter clinical study and review of the literature. Neurosurgery. 2000 Feb. 46(2):282-9; discussion 289-90. [View Abstract]
  61. 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. 1999 Dec. 173(6):1469-75. [View Abstract]
  62. 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. 2007 Aug. 21(4):318-23; discussion 323-7. [View Abstract]
  63. Rinkel GJ. Medical management of patients with aneurysmal subarachnoid haemorrhage. Int J Stroke. 2008 Aug. 3(3):193-204. [View Abstract]
  64. 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. 2001 Jan. 22(1):5-10. [View Abstract]
  65. Rosen DS, Macdonald RL. Subarachnoid hemorrhage grading scales: a systematic review. Neurocrit Care. 2005. 2(2):110-8. [View Abstract]
  66. 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. 2008 Oct. 39(10):2720-6. [View Abstract]
  67. Salary M, Quigley MR, Wilberger JE Jr. Relation among aneurysm size, amount of subarachnoid blood, and clinical outcome. J Neurosurg. 2007 Jul. 107(1):13-7. [View Abstract]
  68. 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. 2008 Jun. 62(6):1236-49; discussion 1249-53. [View Abstract]
  69. Schievink WI. Genetics and aneurysm formation. Neurosurg Clin N Am. 1998 Jul. 9(3):485-95. [View Abstract]
  70. 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. 2006 Jun. 58(6):1054-65; discussion 1054-65. [View Abstract]
  71. Sherlock M, O'sullivan E, Agha A. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf). 2006 Mar. 64(3):250-4. [View Abstract]
  72. Sluzewski M, van Rooij WJ. Early rebleeding after coiling of ruptured cerebral aneurysms: incidence, morbidity, and risk factors. AJNR Am J Neuroradiol. 2005 Aug. 26(7):1739-43. [View Abstract]
  73. Sluzewski M, van Rooij WJ, Beute GN. Late rebleeding of ruptured intracranial aneurysms treated with detachable coils. AJNR Am J Neuroradiol. 2005 Nov-Dec. 26(10):2542-9. [View Abstract]
  74. 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. 1995 Jun. 23(6):1007-17. [View Abstract]
  75. Solomon RA, Fink ME, Pile-Spellman J. Surgical management of unruptured intracranial aneurysms. J Neurosurg. 1994 Mar. 80(3):440-6. [View Abstract]
  76. 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. 2008 Mar. 39(3):899-904. [View Abstract]
  77. Todd MM, Hindman BJ, Clarke WR. Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med. 2005 Jan 13. 352(2):135-45. [View Abstract]
  78. van den Bergh WM, Algra A, van Kooten F. Magnesium sulfate in aneurysmal subarachnoid hemorrhage: a randomized controlled trial. Stroke. 2005 May. 36(5):1011-5. [View Abstract]
  79. 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. 1999 Nov. 91(5):761-7. [View Abstract]
  80. Vespa PM, Gobin YP. Endovascular treatment and neurointensive care of ruptured aneurysms. Crit Care Clin. 1999 Oct. 15(4):667-84. [View Abstract]
  81. 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. [View Abstract]
  82. 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. 2008 Apr. 108(4):832-9. [View Abstract]
  83. 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. 2005 Oct. 128(Pt 10):2421-9. [View Abstract]
  84. White PM, Wardlaw JM, Easton V. Can noninvasive imaging accurately depict intracranial aneurysms? A systematic review. Radiology. 2000 Nov. 217(2):361-70. [View Abstract]
  85. Wiebers DO, Torres VE. Screening for unruptured intracranial aneurysms in autosomal dominant polycystic kidney disease. N Engl J Med. 1992 Sep 24. 327(13):953-5. [View Abstract]
  86. Yuki I, Murayama Y, Vinuela F. Development of medical devices for neuro-interventional procedures: special focus on aneurysm treatment. Expert Rev Med Devices. 2005 Sep. 2(5):539-46. [View Abstract]
  87. 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. 2008 Jul. 63(1 Suppl 1):ONS55-61; discussion ONS61-2. [View Abstract]
  88. 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. 2008 Aug 4. [View Abstract]

Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.

Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.

Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.

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.

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).

Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.

Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.

Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.

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.

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).

Cerebral aneurysms. Clipping vs coiling.

Grade Clinical Condition at Presentation
0Unruptured aneurysm
1Asymptomatic or minimal headache and slight nuchal rigidity
2Moderately severe or severe headache and nuchal rigidity; cranial neuropathy, no focal deficit
3Drowsiness, confusion, or mild focal deficit
4Stupor, moderate to severe hemiparesis
5Deep coma, decerebrate posturing, moribund appearance
Grade Glasgow Coma Scale Score Clinical Findings
I15No headache or focal signs
II15Headache, nuchal rigidity, no focal signs
III13-14Headache, nuchal rigidity, no focal signs
IV7-12Headache, rigidity, focal signs
V3-6Headache, rigidity, focal signs
Grade CT Findings
1No blood detected
2Diffuse thin layer of subarachnoid blood
3Localized thrombus or thick layer of subarachnoid blood
4Intracerebral or intraventricular hemorrhage with diffuse or no subarachnoid blood