Neurosurgery for Cerebral Aneurysm 

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The word aneurysm comes from the Greek word aneurysma (“dilatation”). An aneurysm is an abnormal local dilatation in the wall of a blood vessel, usually an artery, that develops as a consequence of a defect, disease, or injury.

Common causes of intracranial aneurysm include the following:

Uncommon causes include the following:

Aneurysms can be true or false. A false aneurysm is a cavity lined by blood clot. The three major types of true intracranial aneurysms are as follows:

This article reviews the types, pathology, clinical picture, and management of intracranial aneurysms. For patient education resources, see the Headache Center, as well as Aneurysm, Brain.

Saccular aneurysms are rounded berrylike outpouchings that arise from arterial bifurcation points, most commonly in the circle of Willis (see the image below). These are true aneurysms—that is, they are dilatations of a vascular lumen caused by weakness of all vessel wall layers.

A normal artery wall consists of the following three layers:

The aneurysmal sac itself is usually composed of only intima and adventitia. The intima is typically normal, though subintimal cellular proliferation is common. The internal elastic membrane is reduced or absent, and the media ends at the junction of the aneurysm neck with the parent vessel. Lymphocytes and phagocytes may infiltrate the adventitia. The lumen of the aneurysmal sac often contains thrombotic debris. Atherosclerotic changes in the parent vessel are also common.

It was once thought that most saccular or intracranial berry aneurysms were congenital in origin, arising from focal defects in the media and gradually developing over a period of years as arterial pressure first weakened and subsequently ballooned out the vessel wall.

Studies have found scant evidence for congenital, developmental, or inherited weakness of the arterial wall. Although genetic conditions are associated with increased risk of aneurysm development (see below), most intracranial aneurysms probably result from hemodynamically induced degenerative vascular injury. The occurrence, growth, thrombosis, and even rupture of intracranial saccular aneurysms can be explained by abnormal hemodynamic shear stresses on the walls of large cerebral arteries, particularly at bifurcation points.

Less common causes of saccular aneurysms include trauma, infection, tumor, drug abuse (cocaine), and high-flow states associated with AVMs or fistulae.

The incidence of intracranial aneurysm is not known with certainty but is estimated to be in the range of 1-6% of the population. ^[1] Published data vary according to the definition of what constitutes an aneurysm and whether the series is based on autopsy data or angiographic studies. In one series of patients undergoing coronary angiography, incidental intracranial aneurysms were found in 5.6% of cases; another series found aneurysms in 1% of patients undergoing four-vessel cerebral angiography for indications other than subarachnoid hemorrhage (SAH). Familial intracranial aneurysms have been reported. ^[2] Whether this represents a true increased incidence is unclear.

Congenital abnormalities of the intracranial vasculature (eg, fenestrations of the vertebrobasilar junction or persistent trigeminal arteries) are associated with an increased incidence of saccular aneurysms. Fenestrations associated with saccular aneurysms have been found both at the fenestration site and on other, nonfenestrated vessels in the same patient. However, evidence indicates that the incidence of aneurysm at a fenestration site is not different from the typical association of other vessel bifurcations with saccular intracranial aneurysm.

Vasculopathies such as FMD, connective-tissue disorders, and spontaneous arterial dissection are associated with an increased incidence of intracranial aneurysm.

Conditions that have been associated with increased incidence of cerebral aneurysms are as follows:

Autosomal dominant polycystic kidney disease (ADPKD) is by far the most common genetic abnormality associated with intracranial aneurysms, with an estimated 5-40% of ADPKD patients harboring such lesions. ^[3] These lesions are often multiple. All patients with ADPKD should undergo screening with magnetic resonance angiography (MRA). The proper age to begin screening patients with ADPKD and the optimal frequency of rescreening (if the initial MRA findings are negative) are unresolved issues. ^[4]

Screening for intracranial aneurysms is also recommended for people who have two immediate relatives with intracranial aneurysms.

Intracranial aneurysms are multiple in 10-30% of all cases (see the image below). ^[5] About 75% of patients with multiple intracranial aneurysms have two aneurysms, 15% have three, and 10% have four or more. A strong female predilection is observed with multiple aneurysms. Although the overall female-to-male ratio is 5:1, the ratio rises to 11:1 in patients with more than three aneurysms.

Multiple aneurysms are also associated with vasculopathies such as FMD and other connective-tissue disorders.

Multiple aneurysms can be bilaterally symmetric (ie, mirror aneurysms) or located asymmetrically on different vessels. More than one aneurysm can be present on the same artery.

Aneurysms typically become symptomatic in people aged 40-60 years, with the peak incidence of SAH occurring in those aged 55-60 years. ^[6] Intracranial aneurysms are uncommon in children and account for fewer than 2% of all cases. Aneurysms in the pediatric age group are often more posttraumatic or mycotic than degenerative and have a slight male predilection. Aneurysms found in children are also larger than those found in adults, averaging 17 mm in diameter.

Aneurysms commonly arise at the bifurcations of major arteries (see the first image below). Most saccular aneurysms arise on the circle of Willis (see the second image below) or the middle cerebral artery (MCA) bifurcation.

Approximately 86.5% of all intracranial aneurysms arise on the anterior (carotid) circulation. Common locations include the anterior communicating artery (30%), the internal carotid artery (ICA) at the posterior communicating artery origin (25%), and the MCA bifurcation (20%). The ICA bifurcation (7.5%) and the pericallosal/callosomarginal artery bifurcation account for the remainder (4%).

About 10% of all intracranial aneurysms arise on the posterior (vertebrobasilar) circulation. About 7% arise from the basilar artery bifurcation, and the remaining 3% arise at the origin of the posterior inferior cerebellar artery (PICA) where it comes off of the vertebral artery.

Miscellaneous locations account for 3.5% of all lesions and involve sites such as the superior cerebellar artery and the anterior inferior cerebellar artery where they branch off the basilar artery. Saccular aneurysms are uncommon in locations other than the sites mentioned above. Aneurysms that develop at distal sites in the intracranial circulation are often caused by trauma or infection (see Traumatic Aneurysms). Nontraumatic distal aneurysms, particularly along the anterior cerebral artery (ACA), have a high frequency of multiplicity and spontaneous hemorrhage.

Most aneurysms do not cause symptoms until they rupture; when they rupture, they are associated with significant morbidity and mortality.

Subarachnoid hemorrhage

The most common presentation of intracranial aneurysm is SAH (see the images below). In North America, 80-90% of nontraumatic SAHs are caused by the rupture of an intracranial aneurysm. Another 5% are associated with bleeding from an AVM or tumor, and the remaining 5-15% are idiopathic. Remembering that trauma is overwhelmingly the most common cause of SAH is important, and a good history is often helpful in this regard. Increases in the number of patients taking antiplatelet or anticoagulant agents means that even a minor trauma could result in SAH.

On presentation, patients typically report experiencing the worst headache of their lives. The association of meningeal signs should increase suspicion of SAH. For a full description of the SAH, see Subarachnoid Hemorrhage.

Subhyaloid hemorrhages, often bilateral, located between the retina and vitreous membrane, may be observed in as many as 25% of patients. ^[2]

The most widely used clinical method for grading the clinical severity of SAH is the Hunt and Hess scale, which measures the clinical severity of the hemorrhage on admission and has been shown to correlate well with outcome, as follows:

The Fisher grade, which describes the amount of blood seen on noncontrast computed tomography (CT) of the head, is also useful in correlating the likelihood of developing vasospasm (see below), the most common cause of death and disability from SAH. Fisher grades are as follows:

Vasospasm is overwhelmingly most common in Fisher grade 3 and rarely found in patients with no blood on CT. ^[7]

Other symptoms

Signs and symptoms of aneurysm other than those associated with SAH are relatively uncommon. Some intracranial aneurysms produce cranial neuropathies. A common example is the third nerve palsy that is secondary to posterior communicating artery aneurysm. Other, less common symptoms include visual loss caused by an ophthalmic artery aneurysm that compresses the optic nerve, seizures, headaches, and transient ischemic attacks or cerebral infarction secondary to emboli (usually associated with large or giant partially thrombosed MCA aneurysms). So-called giant aneurysms (diameter >2.5 cm) are more often symptomatic because of their mass effect.

Vasospasm is the leading cause of disability and death from aneurysm rupture (see the images below). Of patients with SAH, 10% die before reaching medical attention, and another 50% die within 1 month; 50% of survivors have neurologic deficits. Ruptured aneurysms are most likely to rebleed within the first day (2-4%), and this risk remains very high for the first 2 weeks (~25%) if left untreated.

Three factors that have been correlated with improved outcomes are as follows:

Outcomes associated with unruptured aneurysms are based primarily on whether they are treated and the results of that treatment.

The risk of rupture among aneurysms that have not bled is unknown and for many years was believed to be 1-2% per year. Before the advent of endovascular coiling, most aneurysms were surgically treated via craniotomy (ie, clipped) to prevent a future disastrous hemorrhage. The ISUIA (International Study of Unruptured Intracranial Aneurysms), published in 1998 (retrospective component; N = 2621) and 2003 (prospective component; N =1 692), assessed intracranial aneurysms without intervention to determine the true natural history risk. ^[8] Its findings changed medical understanding of this risk.

Surprisingly, the ISUIA found that for certain aneurysms, particularly those smaller than 7 mm and those located in the anterior circulation in patients who had not had a hemorrhage from another aneurysm, the risk of subsequent rupture was extremely small (0.05%/year in the retrospective arm and a 5-year cumulative risk of rupture of 0% in the prospective arm). ^[8] Aneurysms at other locations (such as the basilar tip and the posterior communicating artery), aneurysms larger than 10 mm, and aneurysms that are found in patients who had bled from a prior aneurysm were found to have higher risks (~0.5%/year).

Despite these results, other reports continued to estimate the rupture risk for unruptured aneurysms at 1% per year. ^[9]  Critics of the ISUIA emphasized that the selection was biased because surgeons who entered patients into the study felt that these aneurysms were less likely to bleed. Nonetheless, the results of this study have significantly affected the way aneurysms are managed, with more and more aneurysms undergoing conservative management as opposed to invasive therapy, particularly if the aneurysms are small and asymptomatic.

Untreated ruptured aneurysms have a very high risk of rebleeding after the initial hemorrhage. The risk is estimated at 20-50% in the first 2 weeks, and such rebleeding carries a mortality of nearly 85%. Aneurysms that have not ruptured but have manifested with other symptoms—for instance, new-onset third nerve palsy (considered a true emergency that necessitates urgent treatment of the aneurysm), brainstem compression due to a giant aneurysm, or visual loss (caused by an ophthalmic artery aneurysm)—should be treated because the natural history risk of rupture is believed to be significantly higher (6%/year) than that of incidentally discovered lesions.

Cigarette smoking, female sex, and younger age have been shown to correlate with aneurysm growth and rupture. ^{[9, 10]}

The apex of vessel bifurcations is the site of maximum hemodynamic stress in a vascular network. Vascular and internal flow hemodynamics have a crucial effect on the origin, growth, and configuration of intracranial aneurysms. In the aneurysm, wall shear stress caused by the rapid changes of blood flow direction (the result of systole and diastole) continually damages the intima at an aneurysm cavity neck. These augmented hemodynamic stresses probably cause the initiation and subsequent progression of most saccular aneurysms. Thrombosis and rupture are also explained by intra-aneurysmal hemodynamic stresses.

Studies demonstrate that the geometric relation between an aneurysm and its parent artery is the principal factor that determines intra-aneurysmal flow patterns. In lateral aneurysms, such as those that arise directly from the ICA, blood typically moves into the aneurysm at the distal aspect of its ostium and exits at its proximal aspect, producing a slow-flow vortex in the aneurysm center. Opacification of the lumen then proceeds in a cranial-to-caudal fashion. Contrast stagnation within these aneurysms is often pronounced.

In contrast to lateral aneurysms, intra-aneurysmal circulation is rapid, and vortex formation with contrast stasis is rare when aneurysms arise at the origin of branching vessels or a terminal bifurcation. These patterns of intra-aneurysmal flow are important not only for the formation and progression of an aneurysm itself but also because they may influence the selection and placement of endovascular treatment devices.

In giant saccular aneurysms (>2.5 cm), slow growth can occur by recurrent hemorrhages into the lesion. The highly vascularized membranous wall of giant intracranial aneurysms is the most likely source of these intra-aneurysmal hemorrhages. Giant sacs commonly contain multilayered laminated clots of varying ages and consistency. The outer wall is fibrous and thick. These multilaminated giant aneurysms seldom rupture into the subarachnoid space and typically produce symptoms related to their mass effect.

Traumatic aneurysms account for fewer than 1% of all aneurysms. The following two general types are identified:

Intracerebral aneurysms secondary to penetrating injuries are commonly due to high-velocity missile wounds of the head. One study demonstrated a 50% overall prevalence of major vascular lesions in civilian patients with penetrating missile injuries examined in the acute stage. Nearly half of these patients had traumatic aneurysms. The diagnosis of posttraumatic aneurysm may be delayed or overlooked on CT because the lesion is often obscured by the presence of an accompanying hemorrhagic intraparenchymal contusion.

Penetrating injuries to extracranial vessels can cause lacerations, arteriovenous fistulae, dissection, or traumatic pseudoaneurysm. The carotid artery is the most frequently involved vessel. Pathologically, a false aneurysm lacks any components of a vessel wall. These false aneurysms, or pseudoaneurysms, are really cavities, typically within adjacent blood clots, that communicate with a vessel lumen. Radiographically, a false aneurysm projects beyond the vessel margin into the adjacent soft tissues. The periadventitial hematoma can be delineated on CT or magnetic resonance imaging (MRI).

Occasionally, the external carotid artery is a site of traumatic injury. The superficial temporal artery (STA) is the most commonly affected vessel. STA traumatic pseudoaneurysm occurs as a complication of scalp trauma and may result from penetrating injury or blunt trauma.

Meningeal vessels are uncommon sites of traumatic pseudoaneurysm development; most occur on branches of the middle meningeal artery. When a meningeal pseudoaneurysm hemorrhages, it is usually into the epidural space. Direct penetrating injury to the vertebral artery (VA) is uncommon. Occasionally, cervical spine fracture-dislocations damage the VA. These typically produce dissection or occlusion; pseudoaneurysms are rare.

Intracranial aneurysm secondary to nonpenetrating trauma is rare and usually occurs at the skull base (where it involves the petrous, cavernous, or supraclinoid ICA) or along the peripheral intracranial vessels. ICA aneurysms at the skull base can be caused by blunt trauma or skull fracture. Hyperextension and head rotation may stretch the ICA over the lateral mass of C1 or shear the artery at its intracranial entrance.

Peripheral intracranial aneurysms can be caused by closed head injury. The distal ACA and peripheral cortical branches are commonly involved sites distal to the circle of Willis. Frontolateral impacts produce shearing forces between the inferior free margin of the falx cerebri and the distal ACA. This can cause a common type of nonpenetrating traumatic intracranial aneurysm, a traumatic aneurysm of the pericallosal artery. Suspect the presence of a traumatic distal ACA aneurysm if a juxtafacial hematoma is observed on CT.

Suspect traumatic cortical artery aneurysm if a delayed hematoma near the brain periphery develops adjacent to the site of a skull fracture.

Although cases have been reported to resolve spontaneously, direct treatment is usually recommended. Such aneurysms can usually be addressed via either a surgical approach (clipping) or an endovascular approach (coiling), depending on the location. For aneurysms located proximally near the skull base, balloon-test occlusion and parent vessel sacrifice may be an option. For distal aneurysms, coiling or clipping with vascular bypass (if important branch vessels are incorporated into the aneurysm neck) may both be considered.

The term mycotic aneurysm refers to any aneurysm that results from an infectious process that involves the arterial wall. These aneurysms may be caused by a septic cerebral embolus that causes inflammatory destruction of the arterial wall, beginning with the endothelial surface. A more likely explanation is that infected embolic material reaches the adventitia through the vasa vasorum. Inflammation then disrupts the adventitia and muscularis, resulting in aneurysmal dilatation.

Mycotic aneurysms were once estimated to account for 2-3% of all intracranial aneurysms but were described as decreasing in the antibiotic era. However, with the increased incidence of drug abuse and immunocompromised states from various causes, mycotic aneurysms may have increased in frequency.

The thoracic aorta has been described as the most common site of mycotic aneurysm. Intracranial mycotic aneurysms are less common. They occur with greater frequency in children and are often found on vessels distal to the circle of Willis. Rarely, deep neck-space infections are complicated by pseudoaneurysm of the cervical ICA.

Mycotic aneurysms generally have a fusiform morphology and are usually very friable. Therefore, treatment is difficult or risky. Most cases are treated emergently with antibiotics, which are continued for 4-6 weeks. Serial angiography (at 1.5, 3, 6, and 12 months) helps document the effectiveness of medical therapy. Even if aneurysms seem to be shrinking, they may subsequently grow, and new ones may form.

Serial MRA may be a viable alternative in some cases. Aneurysms may continue to shrink after completion of antibiotic therapy. Delayed clipping or coiling may be more feasible; indications include the following:

Patients with subacute bacterial endocarditis who require valve replacement should have bioprosthetic (ie, tissue) valves instead of mechanical valves to eliminate the need for risky anticoagulation.

Extracranial oncotic pseudoaneurysms with exsanguinating epistaxis are a common terminal event with malignant head and neck tumors. Intracranial oncotic aneurysms are less common. They are often bizarrely shaped and located on distal branches of the intracranial vessels, remote from the more typical saccular aneurysms located on the circle of Willis.

Oncotic aneurysms may be associated with either primary or metastatic tumors. Neoplastic aneurysms result from direct vascular invasion by a tumor or implantation of metastatic emboli that infiltrate and disrupt the vessel wall. Myxomatous aneurysms are one type of oncotic intracranial aneurysm that are associated with atrial myxomas in a small percentage of cases.

Endovascular treatment using balloon-test occlusion (to determine whether the patient can tolerate vessel sacrifice), followed by intentional vessel occlusion (if the patient passes the test), is one common way to treat such aneurysms. Stent-assisted coiling, in which a porous stent is placed across the aneurysm and is followed by filling the aneurysm with coiling, is another option. Emergency treatment with a covered stent (graft stent) has been used to avert life-threatening intracranial bleeding. (See the images below.)

Intracranial aneurysms associated with primary brain tumors are less common than those caused by metastases. The incidence of saccular aneurysms does not appear to be significantly higher in patients with primary cerebral neoplasms than n the general population, though some authors report a slightly higher incidence with meningiomas.

Metastatic tumors that have been implicated in the development of intracranial aneurysms include left atrial myxoma and choriocarcinoma. Because metastatic tumors are common at the gray-white junction, aneurysms due to metastatic implants often involve peripheral cerebral vessels.

The coexistence of AVMs and aneurysms is well known. The frequency of aneurysms with AVM has been reported as 2.7-30%. Flow-related aneurysms occur along proximal and distal feeding vessels. Proximal lesions arise in the circle of Willis or on vessels that feed the AVM and are probably related to increased hemodynamic stress. No increased frequency of hemorrhage is reported in patients with proximal feeding-artery aneurysms.

Distal flow-related aneurysms are located in distal branches to the AVM. Intranidal aneurysms have been reported in 8-12% of AVMs. These lesions are thin-walled vascular structures without the elastic or muscular layers that characterize arteries. Whether intranidal aneurysms arise from venous ectasias (dilatation) or from the flow-weakened walls of arterial vessels is unclear. Nevertheless, these thin-walled structures are exposed to arterial pressure and are considered a likely site for AVM hemorrhage.

Treatment of aneurysms associated with AVMs is similar to that of aneurysms not associated with AVMs, with the following differences:

Some vasculopathies, such as FMD, have an increased incidence of cephalocervical aneurysms. Some vasculitides, such as systemic lupus erythematosus (SLE) and even Takayasu arteritis, have been associated with aneurysms.

Commonly reported central nervous system (CNS) vascular lesions with SLE include infarcts and transient ischemic attacks. Intracranial hemorrhages are present in approximately 10% of patients with CNS symptoms. Although uncommon, arteritic and nonvasculitic aneurysms occur in SLE. These can be saccular, fusiform, or a bizarre-looking mixture of both.

The characteristic vascular lesions of Takayasu arteritis include occlusion, stenosis, and luminal irregularities, but ectasia and aneurysm formation have also been described in this setting.

Some investigators report a 20-50% incidence of aneurysms in patients with cervical FMD. Other abnormalities associated with FMD include spontaneous dissection, dissecting aneurysms (see below), and arteriovenous fistulae.

Substance abuse, especially with cocaine, can cause certain forms of vasculitis that contribute to aneurysm formation or can cause hemorrhage from preexisting vascular abnormalities such as AVMs or saccular aneurysms because of their ability to cause sudden rapid surges of increased systemic blood pressure to high values.

Cocaine abuse is associated with various CNS complications, including SAH, cerebral ischemia or infarction, intraparenchymal hemorrhage, seizures, vasculitis, vasospasm, and death. Approximately 50% of patients who have a drug abuse problem along with CNS symptoms have SAH; of these, about half have an underlying abnormality such as aneurysm or vascular malformation. Hemorrhage may also be related to the acute hypertensive response that occurs with cocaine use.

Heroin, ephedrine, and methamphetamine use can cause cerebral vasculitis. Necrotizing angiitis, histologically similar to periarteritis nodosa, has been identified in patients who abuse methamphetamines. Focal arterial ectasias, aneurysms, and sacculations have been reported in this form of drug-induced cerebral arteritis.

Fusiform aneurysms are also known as atherosclerotic aneurysms. These lesions are exaggerated arterial ectasias that occur because of a severe and unusual form of atherosclerosis. Damage to the media results in arterial stretching and elongation that may extend over a considerable length. These ectatic vessels may have more focal areas of fusiform or even saccular enlargement. Intraluminal clots are common, and perforating branches often arise from the entire length of the involved parent vessel.

Fusiform aneurysms usually occur in older patients. The vertebrobasilar system is commonly affected. Fusiform aneurysms may thrombose, producing brainstem infarction as small ostia of perforating vessels that emanate from the aneurysm become occluded. They can also compress the adjacent brain or cause cranial nerve palsies.

Fusiform atherosclerotic aneurysms usually arise from elongated tortuous arteries. Patent aneurysms enhance strongly after contrast administration; thrombosed aneurysms are hyperintense on noncontrast CT. Tubular calcification with intraluminal and mural thrombi in the ectatic parent vessels and aneurysm wall is common. Occasionally, fusiform aneurysms cause erosion of the skull base.

On angiography, fusiform aneurysms often have bizarre shapes, with serpentine or giant configurations. Intraluminal flow is often slow and turbulent. These aneurysms typically do not have an identifiable neck. MRI is helpful in delineating the relations between vessels and adjacent structures such as the brainstem and cranial nerves.

In arterial dissections, blood accumulates within the vessel wall through a tear in the intima and internal elastic lamina. The consequences of this intramural hemorrhage vary. If blood dissects subintimally, it causes luminal narrowing or even occlusion. If the intramural hematoma extends into the subadventitial plane, a saclike outpouching may be formed (see image below).

Do not confuse these focal aneurysmal dilatations with the pseudoaneurysms that result from arterial rupture and subsequent encapsulation of the perivascular hematoma. Thus, uncomplicated dissections do not project beyond the lumen of the parent vessel, and dissections with saclike outpouchings are termed dissecting aneurysms. The term false saccular aneurysm, or pseudoaneurysm, should be used for encapsulated, cavitated, paravascular hematomas that communicate with the arterial lumen.

Dissecting aneurysms may arise spontaneously. More commonly, trauma or an underlying vasculopathy such as FMD is implicated.

Most dissecting aneurysms that involve the craniocerebral vessels affect the extracranial segments; intracranial dissections are rare and usually occur only with severe head trauma. Although the common carotid artery (CCA) can be involved by cephalad extension of an aortic arch dissection, the CCA and carotid bulb are usually spared. The ICA is commonly affected. Most dissections involve the midcervical ICA segment and terminate at the extracranial opening of the petrous carotid canal.

The VA is also a common site of arterial dissection. The common location is between the VA exit from C2 and the skull base. Involvement of the first segment, which extends from the VA origin to its entry into the foramen transversarium (usually at the C6 level), is relatively rare.

Dissecting aneurysms are elongated, ovoid, or saccular contrast collections that extend beyond the vessel lumen. Magnetic resonance (MR) studies delineate an intravascular or perivascular hematoma associated with dissections, particularly during the subacute stage. MRA is a helpful screening procedure, but catheter angiography is the procedure of choice for imaging vessel details such as dissection site.

The three major modalities used to reveal and study the size, location, and morphology of an intracranial aneurysm are as follows:

The preferred initial method for evaluation of unruptured intracranial aneurysms is either MRA or CTA, whereas angiography is the preferred modality in patients who have had a subarachnoid hemorrhage (SAH), though CTA alone has been used. ^[11]

Aneurysms that are large enough (usually ≥10 mm) or that contain calcium may be visualized on noncontrast CT and should be sought on any CT scan as a hint to the diagnosis in a patient with an atraumatic SAH. Bone erosion can be observed in long-standing lesions that arise near the skull base. Mural calcification is uncommon, but both punctate and curvilinear types have been identified. The attenuation characteristics of a saccular aneurysm vary, depending on whether the lesion is patent and partially or completely thrombosed.

On noncontrast CT, the typical nonthrombosed aneurysm appears as a well-delineated isodense–to–slightly hyperdense mass located somewhat eccentrically in the suprasellar subarachnoid space or sylvian fissure. Patent aneurysms enhance intensely and quite uniformly following administration of IV contrast material.

Angiogramlike images of the cerebral vasculature can be obtained by using rapid contrast infusion and thin-section dynamic CTA. Various three-dimensional (3D) display techniques, including shaded surface display, volume rendering, and maximal intensity projection, are used to complement the conventional transaxial images. Such studies provide multiple projections of anatomically complex vascular lesions and delineate their relations to adjacent structures (see the image below).

The accuracy of high-resolution axial CT in the diagnosis of cerebral aneurysms 3 mm and larger has been reported to be about 97%.

Partially thrombosed aneurysms have a patent lumen inside a thickened often partially calcified wall that is lined with laminated clot. The residual lumen and outer rim of the aneurysm may enhance strongly following contrast administration. Rarely, atherosclerotic debris in the wall or sac of an aneurysm appears hypodense on CT.

The presence of SAH may complicate the appearance of aneurysms on CT. The reported ability of CT to reveal SAH caused by ruptured cerebral aneurysms in the acute phase is approximately 95%. This sensitivity decreases over time and is somewhat dependent on the CT scanner resolution and the interpreting radiologist. In one study, CT scans detected SAH 100% of the time within 12 hours of the ictus but in only 93% within 24 hours. ^[12]

Acute SAH appears as high attenuation within the subarachnoid cisterns. SAH may quickly spread diffusely throughout the cerebrospinal fluid (CSF) spaces, providing little clue to its site of origin. Suprasellar cistern blood from many sites is common in SAH. However, some bleeding patterns have been associated with particular aneurysm locations.

Hemorrhage located predominantly within the interhemispheric fissure is common in anterior communicating artery aneurysms, and sylvian fissure blood is often observed in MCA lesions. Intraventricular blood can be helpful in localizing ruptured aneurysms. Fourth-ventricle hemorrhage is common in posterior fossa aneurysms, particularly those that arise at the posterior inferior cerebellar artery (PICA) takeoff, and intraventricular blood typically occurs with anterior communicating artery or basilar tip lesions.

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. ^[13]  MRA or CTA was done from age 16-18 years to 65-70 years. Aneurysms were identified in 51 (11%) of 458 individuals at first screening, in 21 (8%) of 261 at second screening, in seven (5%) of 128 at third screening, and in three (5%) of 63 at fourth screening. Five (3%) of 188 individuals without a history of aneurysms and with two negative screens had a de-novo aneurysm in a follow-up screen.

These findings ^[13] suggested that repeated screening should be considered in individuals with two or more first-degree relatives who had SAH or unruptured intracranial aneurysms.

The appearance of an aneurysm on MRI is highly variable and may be quite complex. The signal depends on the presence, direction, and rate of flow, as well as the presence of clot, fibrosis, and calcification within the aneurysm itself.

Patent aneurysms can produce hyperintense or hypointense signals on routine MRI studies, depending on the specific flow characteristics and pulse sequences used. The typical patent aneurysm lumen with rapid flow is visible as a well-delineated mass that shows high-velocity signal loss (flow void) on T1- and T2-weighted images. Some signal heterogeneity may be observed if turbulent flow in the aneurysm is present. Gradient-refocused scans delineate the patent lumen of aneurysms and are particularly helpful when acute thrombus makes the aneurysm difficult to identify.

IV contrast typically does not enhance patent aneurysms with high flow rates, but wall enhancement may occur. Contrast in the intravascular space also often increases artifacts observed with rapid intraluminal flow.

Partially thrombosed aneurysms often have a complex signal on MRI. An area of high-velocity signal loss in the patent lumen with surrounding concentric layers of multilaminated clot and variable signal intensities can be observed. Larger aneurysms may have a thick signal void rim caused by hemosiderin-containing mural thrombus and a hemosiderin-laden fibrous capsule. If intraluminal flow is slow or turbulent, the residual lumen may be isointense with the remainder of the aneurysm and difficult to detect without contrast enhancement.

Completely thrombosed aneurysms also frequently produce variable MRI findings. Subacute thrombus is predominately hyperintense on T1- and T2-weighted studies. Multilayered clots can be observed in thrombosed aneurysms that have undergone repeated episodes of intramural hemorrhage. On occasion, recently thrombosed aneurysms may be isointense with brain parenchyma and difficult to distinguish from other intracranial masses.

The macroscopic motion of the moving spins in flowing blood, together with background suppression of stationary tissue, can be used to create images of the cerebral vasculature. The images can be viewed as individual thin sections (source images) or can be reprojected in the form of flow mapping or MRA (see the image below).

Two standard techniques currently used for MRA include phase-contrast (PC) studies and time-of-flight (TOF) acquisitions. PC creates projection angiographic images by using bipolar pulse sequences to detect the phase shifts caused by blood flowing through magnetic field gradients. PC imaging has excellent background suppression, allows for variable velocity encoding, and can provide directional flow information.

A multislab 3D TOF technique referred to as multiple overlapping thin-section acquisition (MOTSA) combines the advantages of two-dimensional (2D) multiple section and direct 3D TOF techniques. This sequence successfully delineates the parent artery and depicts the size and orientation of an aneurysm dome and neck. Other sequences and future technical refinements will undoubtedly improve MRA delineation of the intracranial vasculature and its lesions.

Catheter-based angiography or digital subtraction angiography (DSA) continues to be the criterion standard for revealing and delineating the features of an intracranial aneurysm. Technologic advances, most notably 3D rotational angiography, have increased the utility of catheter-based angiography for understanding aneurysm anatomy. This technique, popularized in the late 1990s, is now commonly found in modern angiography suites. Images are acquired in 360° and can be rotated in 3D space, giving a more accurate depiction of the aneurysm than 2D angiography can. (See the image below.)

The role of diagnostic cerebral angiography in patients with nontraumatic SAH is to identify the presence of any aneurysms, to delineate the relations of an aneurysm to its parent vessel and adjacent penetrating branches, to define the potential for collateral circulation to the brain, to assess for vasospasm, and, most important, if an aneurysm is encountered, to help determine which treatment modality would best secure the lesion to prevent rebleeding.

Technically adequate cerebral angiography is considered an important and indicated test in the assessment of nontraumatic SAH, though some groups have reported success with CTA as the only diagnostic test before treatment.

When angiography is performed, visualizing the entire intracranial circulation, including the anterior and posterior communicating arteries and both PICAs, is important. Injections with cross-compression, multiple oblique plus submental vertex views and the standard anteroposterior (AP) and lateral projections, and subtraction studies (whether cut film or high-resolution digital) are integral parts of the complete angiographic evaluation.

3D rotational angiography often facilitates a proper understanding of aneurysm morphology, but it may not be available at all institutions. If four-vessel angiography (both carotid injections and both vertebral injections) fails to reveal an aneurysm, six-vessel angiography (including both external carotid injections) to rule out a dural fistula, a rare cause of SAH, should be performed.

A patent intracranial aneurysm is visualized as a contrast-filled outpouching that commonly arises from an arterial wall or bifurcation. The circle of Willis and the MCA bifurcation are common locations. Thrombosed aneurysms occasionally appear normal on angiographic studies. Large thrombosed aneurysms can cause an avascular mass effect.

Aneurysms must be distinguished from vascular loops and infundibuli. Infundibuli are smooth funnel-shaped dilatations that are caused by incomplete regression of a vessel present in the developing fetus. Their most common location is at the origin of the posterior communicating artery from the ICA. Less commonly, an infundibulum arises from the anterior choroidal artery origin. Infundibuli are 2 mm or less in diameter and regular in shape, and the distal vessel exits from their apices.

Vascular loops are caused by overlapping projections of a 3D vessel onto a 2D image; 3D angiography is useful for distinguishing between a loop and a true saccular aneurysm.

When cerebral angiography demonstrates more than one aneurysm, determining which lesion is the most likely rupture site is important. Clinical signs alone are used to localize a ruptured aneurysm in only about one third of these patients. Actual contrast extravasation during angiography is, of course, pathognomonic but extremely rare; rapid hemorrhage within the closed intracranial space is usually fatal.

A focal parenchymal or cisternal hematoma surrounding an aneurysm on CT strongly suggests rupture. Larger, irregularly shaped aneurysms are also more likely to be the offending lesion. Lobulation or a smaller daughter dome (or teat) indicates possible rupture. Although focal vasospasm is a helpful finding, subarachnoid blood quickly spreads along the basal cisterns, making this a somewhat less reliable sign of aneurysm rupture. Positively determining the ruptured aneurysm is sometimes impossible. Clinical decision-making is needed to determine which aneurysm or aneurysms require treatment in the acute setting.

In approximately 15% of patients with nontraumatic SAH, no aneurysm is found despite a complete, high-quality, six-vessel cerebral angiogram. Two distinct subsets of these patients have been recognized. The first group consists of those with so-called benign perimesencephalic nonaneurysmal SAH (BPNSAH), in which bleeding on CT or MRI is localized immediately anterior to the brainstem and adjacent areas such as the interpeduncular fossa and ambient cisterns.

Findings on initial and follow-up angiography are almost always negative in BPNSAH patients, and their prognosis is excellent. In these cases, SAH probably results from spontaneous rupture of small pontine or perimesencephalic veins, and one catheter angiogram is usually sufficient if the pattern of blood on CT is truly small and localized as described above. With increasing resolution of high-powered multislice CT scanners using CTA, a 2007 report suggests that this is a sufficient test for BPNSAH, ^[14]  but evidence is insufficient to support this strategy at present, and DSA is indicated.

In the second group with angiogram-negative SAH, CT reveals an aneurysmal pattern of hemorrhage (ie, blood fills the suprasellar cistern, extends into the lateral sylvian or anterior interhemispheric fissures, or does both). The risk of rebleeding, hydrocephalus, delayed cerebral ischemia from vasospasm, and neurologic deficit is about as high in this group as when an aneurysm is found and warrants repeat angiography (1-6 weeks later) to identify an occult aneurysm that may have initially been compressed by the hematoma or did not opacify because of local vasospasm.

Repeat four-vessel cerebral angiography demonstrates a lesion in 10-20% of these cases. MRI with gadolinium of the brain and cervical spine is also indicated to rule out vascular abnormality or tumor as the cause of the bleed.

This section highlights the basic principles of aneurysm treatment. Management of SAH is discussed more fully elsewhere (see Subarachnoid Hemorrhage). Guidelines for the management of SAH based on levels of evidence have been published by the American Heart Association (AHA) and the American Stroke Association (ASA). ^[15]  Future developments in the treatment of cerebral aneurysm and SAH are likely to rely increasingly on so-called personalized medicine. ^[16]

Treatment decisions for ruptured aneurysms differ significantly from those for unruptured aneurysms. Ruptured aneurysms should be treated urgently (≤ 72 hours of hemorrhage) to prevent rebleeding and to permit aggressive management of vasospasm. Unruptured aneurysms are generally treated electively. The following are three options for treating intracranial aneurysms:

In the earlier days of aneurysm treatment, surgery was delayed until the second or third week after the hemorrhage to avoid difficulty related to brain swelling during surgery. Although this reduced surgical morbidity and mortality, results were not always good, because of a high incidence of rebleeding and difficulty in managing vasospasm. Although how to treat patients with a very poor grade (grade 5) is controversial, current recommendations are that select patients in this group undergo aneurysm treatment; coiling has become a good alternative for this subset of patients.

Administer calcium-channel blockers (nimodipine for 21 days) to all patients; this has been shown to improve outcomes after SAH. ^[17]  Although studies of the effect of nimodipine on vasospasm have shown different results, this agent is currently recommended as first-line medical treatment for preventing cerebral vasospasm after aneurysmal SAH. ^[15]  Anticonvulsant use is controversial, but is generally given (levetiracetam or phenytoin), particularly for patients undergoing craniotomy or those with focal cerebral hematomas in addition to the SAH.

Blood in the subarachnoid space obliterates the arachnoidal villi, causing acute hydrocephalus. Blood within the ventricles can block the foramen of Monroe, also leading to hydrocephalus. When hydrocephalus leads to neurologic worsening because of the raised intracranial pressure (ICP), a ventriculostomy catheter should be emergently placed for CSF diversion. Not only can this be lifesaving, but a patient’s neurologic examination can improve dramatically after the hydrocephalus has been treated.

Whether to treat or not is a dilemma that applies only to unruptured aneurysms; all ruptured aneurysms should be treated to avoid disastrous rebleeding (rare exceptions may include hemodynamic instability, extreme old age, or a clinical condition approaching brain death). Cerebral aneurysms are increasingly revealed before rupture because of the advances and ready availability of noninvasive neuroimaging techniques.

With the increased ability to reveal aneurysms early comes the need to identify which incidentally revealed aneurysms should be treated and with what modality. A decision to treat is individualized and should be made by a physician or physicians who are capable of offering both modalities of treatment, clipping or coiling, without bias. Although only neurosurgeons currently perform clipping, coiling is performed by interventional neuroradiologists or neurosurgeons or neurologists with endovascular training.

The risks of any proposed treatment must outweigh the natural history risks or risk associated with no treatment. Risks of treatment and no treatment vary depending on many patient-specific and aneurysm-specific factors, including aneurysm size, location, and morphology and patient age and medical comorbidities.

One treatment strategy is outlined in an algorithm (see the image below). In general, a life expectancy of 10 years or longer would warrant treatment of unruptured incidental aneurysms in elderly patients or in those who have a terminal ailment. Of course, exceptions exist, and as endovascular technology increases and hopefully becomes even safer, this recommendation may change.

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. ^[18]

In this study, long-term occlusion was achieved in 79% of patients. ^[18] 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.

Anxiety in patients who know they have an aneurysm can have a substantial influence on treatment decisions. The patient’s feelings, experiences, biases, and personal preferences are important. Many patients choose against surgery because they place more weight on avoiding its risks (eg, death and disability) than on preventing the possibility of future rupture. On the other hand, some patients are so frightened by knowing that they have an aneurysm (patients have referred to aneurysms as “a time bomb ticking in my head”) that they cannot function until it is repaired.

The true natural history risk of rupture of an incidentally discovered aneurysm is unknown. A substantial contribution to our understanding was made by the International Study of Unruptured Intracranial Aneurysms (ISUIA), in which 2621 subjects from 53 centers with unruptured aneurysms were studied conservatively. ^[8] The risk of rupture for certain small aneurysms was significantly smaller than what would have been predicted (0.05% per year risk of rupture).

The study also had a prospective arm in which 1692 patients with unruptured aneurysms were studied. The results were similar, with patients who harbored small aneurysms (< 7 mm) in certain locations in the anterior circulation having a 5-year cumulative risk of rupture of 0%. Of course, as the aneurysms grew and were associated with previously ruptured aneurysms in the same patient, and when the aneurysms were located at different locations (basilar tip, posterior communicating), the risk increased significantly. The 5-year risk of rupture in patients with posterior communicating aneurysms that were 13-25 mm, for example, was 18.4%. ^[1]

The study also analyzed surgery-related morbidity and mortality among 1172 patients with newly diagnosed unruptured intracranial aneurysm. The outcome of surgery depended heavily on age. The combined rate of surgery-related morbidity and mortality at 1 year for patients without prior SAH was 6.5% in patients younger than 45 years, 14.4% in those aged 45-64 years, and 32% in patients older than 64 years. The authors concluded that the risks of surgery outweighed the benefits in patients without previous subarachnoid bleeding who had aneurysms smaller than 10 mm in diameter.

In the Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage, which involved 6038 ruptured aneurysms, the critical size of rupture was found to be 7-10 mm. Other studies of large personal or institutional series have recorded higher rates of rupture for unruptured aneurysms. ^{[9, 19]}

The decision regarding whether to treat an unruptured intracranial aneurysm can require great wisdom. Physicians should review all the relevant data from trials and natural history studies. They must also become acquainted with their patients and their particular conditions, coexisting disorders, and desires. Some patients welcome statistical data and choose therapies logically on the basis of such data. Others eschew science and rely on alternative therapies. Decisions take time, patience, experience, and repeated visits with patients.

Obliteration of an aneurysm (ruptured or unruptured) with endovascular coiling or surgical clipping is a matter of much controversy. Currently, data suggest that whereas coiling is somewhat safer than clipping for both ruptured and unruptured aneurysms, at least in the acute perioperative period, clipping is slightly more durable.

Risks

Exact risks for clipping or coiling an aneurysm are not known and depend on patient and aneurysm specific factors. Surgeon and institutional volume likely also plays a role, which has not yet been quantified. ^{[20, 21, 22]}

Historical data published by experienced vascular surgeons suggest that the morbidity and mortality figures associated with clipping an unruptured aneurysm are 4-10.9% and 1-3%, respectively. ^{[23, 24, 25]} The ISUIA also examined the risks associated with clipping an unruptured aneurysm and found that those risks (15.7% morbidity at 1 year) were higher than previously believed. 

Estimated risks associated with coiling based on several large studies are on the order of 3.7-5.3% morbidity and 1.1-1.5% mortality. ^{[26, 27]}  A major drawback associated with coiling is that over time, the coils can compact, leading to reopening or recanalization of the aneurysm. A reopened aneurysm has a certain risk of hemorrhage, the magnitude of which is not known. Fortunately, repeat coiling is a fairly safe technique. Additionally, newer technologic advances such as newer biologically active coils and stents designed to prevent recanalization have been developed, and the early results are encouraging.

Surgical clipping vs endovascular coiling

Several studies have attempted to compare the two techniques and have found coiling to be safer but slightly less durable. Studying the California statewide database, Johnston et al found that outcomes after clipping unruptured aneurysms were significantly worse than those following coiling; coiling was also associated with lower inpatient mortality, shorter lengths of hospital stays, and lower costs. ^[28]

Increased safety of coiling over clipping was better demonstrated in the well-publicized International Subarachnoid Aneurysm Trial (ISAT) conducted in England. ^[29]  In that study, 2143 patients who presented with SAH and were deemed to have an aneurysm that was felt to be treatable with either coiling or clipping were prospectively randomized to one of the two treatments. The study was stopped prematurely after a planned interim analysis found a 23.7% rate of dependency or death in the coiling cohort versus a 30.6% rate in the clipping cohort.

This controversial study significantly affected the treatment of ruptured aneurysms. The main criticism of the study was that the great majority of the aneurysms were felt to be better treated by one modality over the other and were therefore not randomized. Only 22.4% of all aneurysms screened were randomized. Of those, the overwhelming majority were small and located in the anterior circulation. Therefore, although the ISAT is important, generalizing the results to all ruptured aneurysms is not appropriate.

Continued follow-up from the ISAT confirmed the original results with a higher rate of seizures in the clipping group and a slightly higher rate of rebleeding in the coiling group. ^[30]  Subsequently, the ISAT investigators reported on a reanalysis of the data in which they stratified the benefit of coiling over clipping in patients with SAH. ^[31] Because of the small chance of aneurysm recurrence (recanalization) after coiling that is higher than with clipping, the investigators found that the results of the study may not necessarily apply to patients younger than 40 years.

In a review of hospital mortality associated with elective treatment of unruptured intracranial aneurysms, Alshekhlee et al found that endovascular coiling was associated with a lower death rate than surgical clipping (0.57% vs 1.6%), as well as lower rates of perioperative intracerebral hemorrhage and acute ischemic stroke. During the years 2000 through 2006, a trend toward greater use of endovascular coiling procedures was observed. ^[32]

A prospective multicenter study by Hammer et al (N = 661), designed to compare the results of endovascular treatment of ruptured intracranial aneurysms (n = 271) with those of microsurgical clipping (n = 390), found that the latter was associated with a lower rate of modality-associated complications and a higher occlusion rate of ruptured aneurysms. ^[33]

Ultimately, the decision to clip or coil should be made on an individual basis and may often involve difficult to quantify variables such as patient interest in one technique over the other or the experience or availability of physician operators.

Controversy exists with respect to whether so-called early surgery (generally, but not precisely, defined as ≤48-96 hours after SAH) or late surgery (usually >10-14 days after SAH) should be recommended.

Early surgery is advocated for the following reasons:

Arguments against early surgery and in favor of late surgery include the following:

Although no randomized trials have compared early surgery and late surgery, the trend in the United States has been strongly toward early surgery. The advent of endovascular coiling as a less invasive modality of treatment that does not require brain manipulation is expected to continue the ability to treat patients in the early period.

The goal of surgical treatment is usually to place a clip across the neck of the aneurysm to exclude the aneurysm from the circulation (see the image below) without occluding normal vessels.

When the aneurysm cannot be clipped because of the nature of the aneurysm or the poor medical condition of the patient, and the aneurysm is felt not to be a candidate for endovascular therapy (see below), the following alternatives may be considered:

Although wrapping should never be the goal of surgery, situations may arise in which little else is possible (eg, fusiform basilar trunk aneurysms). Plastic resins may be slightly better than muscle or gauze for this purpose. Wrapping can be performed with cotton or muslin, with muscle, or with plastic or other polymer. Some studies demonstrate benefit with plastic or other polymer, but others show no difference from natural course. In one study with long-term follow-up, the protection from rebleeding during the first month was unchanged, but thereafter, the risk was slightly lower than for the natural history.

Trapping may be warranted in some cases. Effective treatment requires both distal and proximal arterial interruption with direct surgery (ligation or occlusion with a clip). Treatment may also incorporate extracranial-intracranial (EC-IC) bypass to maintain flow distal to the trapped segment.

Proximal ligation has been used with some success for giant aneurysms, particularly of the vertebrobasilar circulation. Advanced endovascular techniques, however, now offer better alternatives for such lesions.

After performing a craniotomy, use microsurgical techniques with the operative microscope to dissect the aneurysm neck free from the feeding vessels without rupturing the aneurysm. Final treatment involves the placement of a surgical aneurysm clip around the neck of the aneurysm, thereby obliterating the flow into the aneurysm. The goal at surgery is to obliterate the aneurysm from the normal circulation without compromising any of the adjacent vessels or small perforating branches of these vessels. The clips are available in various types, shapes, sizes, and lengths and are manufactured so as to be compatible with MRI.

Intraoperative angiography is now frequently used as an adjunct to clipping and permits confirmation of aneurysm occlusion and patency of nearby vessels. The frequency of its use varies widely; however, many vascular neurosurgeons choose to use this technique selectively for difficult aneurysms.

A technique called near-infrared indocyanine green videoangiography (ICGA) has gained some popularity as a less invasive way of assessing aneurysm and blood-vessel patency during aneurysm surgery. ^[34] After IV injection of the indocyanine green dye, an operating microscope equipped with appropriate software can within minutes detect blood flow within the vasculature using near infrared technology (see the video below). The technique is less invasive than intraoperative angiography, but one disadvantage is that only vessels that can be seen by the operating microscope can be evaluated.

The operative morbidity and mortality associated with clipping depends on whether the aneurysm has ruptured; ruptured aneurysms are more treacherous to operate on, and morbidity is higher. Surgery for unruptured aneurysms is estimated to be associated with a 4-10.9% morbidity and a 1-3% mortality. ^{[35, 25]} Many factors affect morbidity, with larger aneurysms in certain locations and in older, less medically healthy patients faring less well.

Surgeon experience likely plays a role as well, with high-volume surgeons working in high-volume institutions likely having lower morbidity; however, the definition of high-volume is a subject of controversy. Excellent clinical outcomes from one low-volume hospital’s experience with clipping unruptured aneurysms suggest that outcomes after clipping are multifactorial. ^[36] The exact contribution of surgeon or hospital volume remains unclear.

The details of the sophisticated surgical approaches and techniques used to explore and dissect in order to clip the various aneurysms are beyond the scope of this review.

Most agree that angiography is necessary after surgery to confirm good clip placement with total obliteration of the aneurysm and patency of the surrounding vessels. In cases where these objectives are achieved, the rebleeding rate is negligibly low.

Whether a patient who undergoes intraoperative angiography should undergo postsurgery angiography with the better equipment available in a dedicated angiography suite is also controversial, and practices vary.

After successful obliteration of a ruptured aneurysm, the patient remains at significant risk for vasospasm, hydrocephalus, and medical complications (including hyponatremia, venous thromboembolism, infections, and cardiac stun) and remains in an intensive care setting for at least 7-10 days. ^[37] Operative complications represent only a small portion of the morbidity and mortality associated with a ruptured intracranial aneurysm. The major causes of morbidity and mortality include misdiagnosis, rebleeding, hydrocephalus, and vasospasm.

Vasospasm is defined as angiographic narrowing that can lead to delayed ischemia. Clinically, it is diagnosed as deterioration in mental status or focal neurologic deficits, most commonly hemiparesis or dysphasia. Transcranial Doppler ultrasonography (TCD) is frequently used as a noninvasive diagnostic tool and is sensitive to changes in the vessel caliber of the larger vessels of the circle of Willis. A trained technician should perform TCD daily or every other day during the vasospasm period (days 3-12 after SAH, with some flexibility, depending on the extent of the hemorrhage).

If the patient’s condition deteriorates, excluding all other causes of neurologic deterioration is important. If in doubt, cerebral angiography is indicated to confirm the diagnosis. Vasospasm must be aggressively managed once it is detected because it can lead to permanent disability and death.

So-called triple-H therapy (hypertension, hemodilution, and hypervolemia) remains the most important aspect of the medical management of vasospasm, but in refractory cases where medical management fails, endovascular methods are warranted. Transluminal balloon angioplasty is the primary method of choice, but intra-arterial papaverine may be used for vasospasm in the distal vasculature, which may not be accessible to balloons. Additionally, intra-arterial papaverine may be used to temporarily open vessels to permit passage of a balloon, which can then be used to treat the vasospasm. Papaverine has been shown to be short-lived and associated with more adverse side effects than angioplasty. ^[38]

Persistent hydrocephalus develops in approximately 20% of cases. In such instances, a shunting procedure, usually a ventriculoperitoneal shunt, is required.

Various endovascular methods have been developed and refined to treat intracranial aneurysms. Initially, endovascular balloon occlusion of a feeding artery was performed. However, this procedure was soon followed by direct obliteration of the aneurysmal lumen, first by detachable balloons and later by microcoils. Guglielmi et al described a detachable platinum microcoil for use in treatment of intracranial aneurysms. These coils are soft and can be detached from the stainless steel guide by passing a very small direct current that causes electrolysis at the solder junction. Separation usually occurs within 2-10 minutes after satisfactory coil placement.

Since the approval of this device by the US Food and Drug Administration (FDA) in 1995, coiling has become the primary treatment modality of aneurysms in many centers. Whereas coiling was initially used for aneurysms not amenable to surgical clipping, it can now be used to treat most aneurysms. Previous limitations, such as inability to coil aneurysms with wide necks or complex morphologies and high rates of recurrence secondary to coil compaction, have been addressed with complex-shaped coils, balloon and stent technology, and biologically active coils.

Accumulating experience with some of the biologically active coils and stents has made it clear that these advanced endovascular techniques, though of some increased benefit, may also be associated with new and increased risks. Such risks must be evaluated in regard to potential benefits and alternative strategies.

The Hydrocoil (Microvention, Inc), a biologically active coil, has been associated with a small incidence of aseptic meningitis and hydrocephalus. ^[39]  The Neuroform stent (Target, Boston Scientific), which has rendered many aneurysms amenable to endovascular therapy that otherwise would not have been, requires the use of clopidogrel bisulfate for 6-12 weeks post procedure and has been associated with an in-stent stenosis rate of 5.8% in short- to medium-term follow-up. Fortunately, most of the stenoses are asymptomatic and often resolve over time. ^[40]

The coils most commonly used in endovascular procedures are platinum Guglielmi detachable coils (GDC). The purpose of the coil is to induce thrombosis at the site of deployment via electrothrombosis. Biologically active coils are coated with various substances to enhance permanency of the thrombus within the coiled aneurysm by permitting a denser packing or engendering a tissue response at the neck of the aneurysm that decreases blood flow into the aneurysm and subsequent recanalization.

Electrothrombosis occurs because white and red blood cells, platelets, and fibrinogen are negatively charged. If a positively charged electrode is placed in the bloodstream, it attracts these negatively charged blood components, promoting clot formation.

Platinum is used for electrothrombosis because unlike metals with a high dissociation constant, the positive end does not dissolve. Furthermore, platinum is three to four times more thrombogenic than stainless steel is. The platinum coil is delivered via a stainless steel delivery system, which is detached by electrolysis.

Numerous experimental and human series indicated that the thrombotic reaction induced by electrothrombosis is not complete. Thus, the coil surface is being modified to enhance the thrombogenic potential of the procedure. Arterial access is achieved via percutaneous puncture of the femoral artery. A heparin bolus is administered intravenously to achieve an activated coagulation time (ACT) longer than 250 seconds in patients with unruptured aneurysms. Patients with ruptured aneurysms may not receive any heparin until the first coil is deployed, but, again, practice patterns differ greatly.

For each embolization procedure, a guide catheter is placed in the cervical ICA or the VA. Microcatheters of varying sizes can then be navigated into the aneurysm cavity by using magnified road-mapping technique.

A microcatheter that contains two radiopaque markers is advanced into the aneurysm cavity. Coils of decreasing sizes are delivered into the aneurysm cavity and electrolytically detached (though some newer generation coils involve detachment strategies that do not involve electrolysis). Angiograms are obtained before each coil is detached to ensure preservation of the parent vessel. This process is continued until maximal angiographic obliteration of the aneurysm cavity is achieved.

For aneurysms with a wide neck, coils can protrude into the parent vessel and can compromise the artery. Balloon-assisted and stent-assisted GDC placements have been used in such patients (see the images below).

Stent-assisted coiling for the treatment of wide-neck aneurysms has been used more often. ^[41] Various self-expandable stents specifically designed for intracranial use exist; Neuroform (Boston Scientific), Enterprise (Cordis), and LVIS and LVIS Jr (MicroVention) have all been FDA-approved for use in the United States.

Experimental and clinical evidence suggests that stent placement across the neck of an aneurysm causes a hemodynamic flow diversion that can, on occasion, cause aneurysmal occlusion/thrombosis without the need to introduce coils. Such stents are referred to as vascular reconstruction devices (VRDs).

One such stent with a more tightly constructed mesh, Pipeline (eV3), designed to cause increased hemodynamic diversion relative to the aforementioned self-expandable stents, gained FDA approval in the United States, and several reports on its use in patients have been published. ^{[42, 43, 44, 45]}  A similar VRD, the SILK stent (Balt), was approved in Europe but not in the United States. The Surpass (Stryker) received premarket approval from the FDA in May 2018.

These stents routinely cause sufficiently decreased flow into the aneurysm as to obviate the need for adjunctive coiling, though simultaneous coiling can be performed if necessary. Such stents have permitted treatment of certain fusiform and giant aneurysms that had no reasonable alternatives.

However, the complication rates associated with their use appear higher than with other endovascular devices. Routine complications include thromboembolic events and in-stent stenosis. More unique and not readily understood complications (eg, delayed rupture of previously unruptured aneurysms and intracerebral hemorrhage distal to the treated lesion) have been reported. ^[46]  Thus, such devices must be used with extreme caution, particularly in aneurysms for which less risky alternative treatments with better-defined complication profiles are available.

In a May 2018 letter to healthcare providers, the FDA provided recommendations on the use of neurovascular stents used for stent-assisted coiling of brain aneurysms, noting the risks of such treatment and emphasizing that patients must be appropriately selected and the devices properly deployed to ensure that the benefits of therapy outweigh the risks. ^[47]

In a prospective, multicenter, single-arm, open-label study of 30 patients with unruptured wide-necked intracranial aneurysms who were treated with the newer-generation Neuroform Atlas stent and approved coils, Jankowitz et al reported a high rate of complete aneurysm occlusion at 12-month angiographic follow-up, with an improved safety profile. ^[48]

Endovascular coiling continues to be a very popular approach to treating aneurysms. As experience accumulates, more and more aneurysms that previously were treated with clipping are undergoing endovascular therapy with both success and safety. Specifically, very small aneurysms (less than 2-3 mm in maximal diameter) have been successfully coiled with relative safety and efficacy in large series. ^[49]

Endovascular treatment of cerebral aneurysms has been reported to have a higher recurrence rate than microsurgical clip ligation. A single-center study by Liu et al suggested that microsurgical clip ligation might be the treatment of choice for certain recurrent aneurysms that were previously treated with endovascular coiling (with or without the assistance of stents). ^[50]

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Jonathan L Brisman, MD Consulting Staff, Neurological Surgery, PC; Director, Cerebrovascular and Endovascular Neurosurgery, Winthrop University Hospital

Jonathan L Brisman, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

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.

Ryszard M Pluta, MD, PhD Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences, Poland; Clinical Staff Scientist, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH); Fishbein Fellow, JAMA

Ryszard M Pluta, MD, PhD is a member of the following medical societies: Polish Society of Neurosurgeons, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Brian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai

Brian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons, International Parkinson and Movement Disorder Society, North American Neuromodulation Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from Abbott Neuromodulation for consulting.

Paul L Penar, MD, FACS Professor, Department of Surgery, Division of Neurosurgery, Director, Functional Neurosurgery and Radiosurgery Programs, University of Vermont College of Medicine

Paul L Penar, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, World Society for Stereotactic and Functional Neurosurgery, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Abraham Kader, MD Consulting Surgeon, Department of Neurosurgery, Virginia Hospital Center

Abraham Kader, MD is a member of the following medical societies: American Association of Neurological Surgeons, Medical Society of the State of New York, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Norvin Perez, MD Medical Director, Juneau Urgent and Family Care

Norvin Perez, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association

Disclosure: Nothing to disclose.

Emad Soliman, MD, MSc Consulting Staff, Department of Neurology, St John’s Riverside Hospital

Emad Soliman, MD, MSc is a member of the following medical societies: American Academy of Neurology and American Medical Association

Disclosure: Nothing to disclose.

Neurosurgery for Cerebral Aneurysm 

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