Cerebral Aneurysm

INTRODUCTION

The word aneurysm comes from the Latin word aneurysma, which means dilatation. Aneurysm is an abnormal local dilatation in the wall of a blood vessel, usually an artery, due to a defect, disease, or injury.

Aneurysms can be true or false. A false aneurysm is a cavity lined by blood clot. The 3 major types of true intracranial aneurysms are saccular, fusiform, and dissecting.

This article reviews the types, pathology, clinical picture, and management of intracranial aneurysms.

Pathology

Saccular aneurysms are rounded berrylike outpouchings that arise from arterial bifurcation points. These are true aneurysms, ie, they are dilatations of a vascular lumen caused by weakness of all vessel wall layers.

A normal artery wall consists of 3 layers: the intima, which is the innermost endothelial layer; the media, which consists of smooth muscle; and the adventitia, the outermost layer, which consists of connective tissue. The aneurysmal sac itself is usually composed only of intima and adventitia. The intima is typically normal, although 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. Thrombotic debris is often present in the lumen of the aneurysmal sac. Atherosclerotic changes in the parent vessel are also common.

Etiology

In the past, most saccular or intracranial berry aneurysms were thought to be congenital in origin, arising from focal defects in the media and gradually developing over a period of years as arterial pressure first weakens and subsequently balloons out the vessel wall.

Recent 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.

Incidence

The true incidence of intracranial aneurysm is unknown. 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, and another series found aneurysms in 1% of patients undergoing 4-vessel cerebral angiography for indications other than subarachnoid hemorrhage (SAH). Familial intracranial aneurysms have been reported, but whether this represents a true increased incidence is unclear.

Associated conditions

Congenital abnormalities of the intracranial vasculature, such as anomalous vessels, are associated with an increased incidence of saccular aneurysms. Arterial fenestrations have been reported with saccular aneurysms both at the fenestration site and on other, nonfenestrated vessels in the same patient. However, recent evidence indicates that 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 fibromuscular dysplasia (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:

• Anomalous vessels

• Coarctation of the aorta

• Polycystic kidney disease

• FMD

• Connective tissue disorders (eg, Marfan, Ehlers-Danlos)

• High-flow states (eg, vascular malformations, fistulae)

• Spontaneous dissections

Multiplicity

Intracranial aneurysms are multiple in 15-20% of all cases (see Image 3). About 75% of patients with multiple intracranial aneurysms have 2 aneurysms, 15% have 3, and 10% have more than 3. A strong female predilection is observed with multiple aneurysms. While the overall female-to-male ratio is 5:1, the ratio rises to 11:1 in patients with more than 3 aneurysms.

Multiple aneurysms are also associated with vasculopathies such as FMD and other connective tissue disorders. Polycystic kidney disease has a 10% incidence of associated aneurysms; these aneurysms are also often multiple.

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

Age at presentation

Aneurysms typically become symptomatic in people aged 40-60 years. Intracranial aneurysms are uncommon in children, accounting for fewer than 2% of all cases. When aneurysms occur in the pediatric age group they are more often posttraumatic or mycotic than degenerative, and they have a slight male predilection. Aneurysms in children are also larger than those found in adults, averaging 17 mm in diameter.

Location

Aneurysms commonly arise at the bifurcations of major arteries. Most saccular aneurysms arise on the circle of Willis (see Images 1-2) or the middle cerebral artery (MCA) bifurcation.

• Anterior circulation aneurysms: Approximately 85% of all intracranial aneurysms arise on the anterior (carotid) circulation. Common locations are the anterior communicating artery (30-35%), the internal carotid artery (ICA) at the posterior communicating artery origin (30-35%), and the MCA bifurcation (20%).

• Posterior circulation aneurysms: About 15% of all intracranial aneurysms arise on the posterior (vertebrobasilar) circulation. Five percent arise from the basilar artery bifurcation, and the remaining 1-5% arise from other posterior fossa vessels. Common posterior fossa sites include the superior cerebellar artery and the vertebral artery (VA) at the origin of the posterior inferior cerebellar artery (PICA). Anterior inferior cerebellar artery (AICA) aneurysms are rare.

• Miscellaneous locations: Saccular aneurysms are uncommon in locations other than the circle of Willis, the MCA bifurcation, or the pericallosal artery origin. When aneurysms occur at distal sites in the intracranial circulation, they are often caused by trauma or infection. Nontraumatic distal aneurysms, particularly along the anterior cerebral artery (ACA), have a high frequency of multiplicity and spontaneous hemorrhage.

Clinical presentation

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 Image 5 and Image 8). In North America, 80-90% of nontraumatic SAHs are caused by rupture of an intracranial aneurysm. Another 5% are associated with bleeding from an AVM, and the remaining 15% are idiopathic.

  • On presentation, patients typically report experiencing the worst headache of their lives. The association of meningeal signs should increase suspicion of SAH. 

  • The most widely used clinical method for grading the clinical severity of SAH is the Hunt and Hess scale.
    • Grade 0 - Unruptured aneurysm

    • Grade 1 - Asymptomatic or minimal headache and slight nuchal rigidity

    • Grade 1A - No acute meningeal or brain reaction but with fixed neurologic deficit

    • Grade 2 - Moderate-to-severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy

    • Grade 3 - Drowsiness, confusion, or mild focal deficit

    • Grade 4 - Stupor, moderate-to-severe hemiparesis, possible early decerebrate rigidity, and vegetative disturbances

    • Grade 5 - Deep coma, decerebrate rigidity, and moribund appearance

  • Another grading system for SAH is the Cooperative Aneurysm Study Neurological Status Scale.
    • Status 1 - Symptom free

    • Status 2 - Minor symptoms

    • Status 3 - Major neurologic deficit but fully responsive

    • Status 4 - Impaired state of alertness but capable of protective or adaptive responses to noxious stimuli

    • Status 5 - Poorly responsive but with vital signs

    • Status 6 - No response to shaking, nonadaptive responses to stimuli, and progressive instability of vital signs

  • 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 third nerve palsy secondary to posterior communicating artery aneurysm. Cavernous ICA aneurysms can compress nerves III-VI. Other less common symptoms include intracerebral hemorrhage (see Image 6 and Image 9), partial visual loss caused by an ophthalmic artery aneurysm compressing the optic nerve, seizures, headaches, and transient ischemic attacks or cerebral infarction secondary to emboli. The so-called giant aneurysms (diameter >2.5 cm) are more often symptomatic because of their mass effect.

Clinical outcome

Vasospasm is the leading cause of disability and death from aneurysm rupture (see Image 4). Of patients with SAH, 10-15% die, 50% of whom die within a month, and 50% of survivors have neurological deficits. Ruptured aneurysms have their highest rebleeding rate within the first day; if untreated, at least 50% rebleed during the 6 months after the initial hemorrhage. Ultra-early referral, the earliest possible surgery, and aggressive anti-ischemic treatment (ie, antivasospastic drugs, intravascular volume expansion, transcranial doppler monitoring) gradually are improving the outcome.

Natural history

The risk of aneurysm rupture is difficult to determine precisely but is estimated at 1-2% per year, cumulative, for asymptomatic lesions that have not yet ruptured. With a combined operative mortality rate and major morbidity risk of about 3.5% for aneurysm surgery performed by a skilled physician, recent conclusions are that any patient with a life expectancy of more than 3 years would benefit from surgical obliteration of an unruptured asymptomatic aneurysm.

Ruptured aneurysms that are not operated on have a very high risk of rebleeding after the initial hemorrhage has occurred. The risk is estimated at 20-50% in the first 2 weeks, and such rebleeding carries a mortality rate of nearly 85%.

No consensus exists regarding the risks associated with unruptured aneurysms. The size of an intact saccular aneurysm as observed on cerebral angiography is an important (but not absolute) determinant of the risk of aneurysmal rupture. In one long-term study, all aneurysms that subsequently ruptured were larger than 10 mm in diameter, although a follow-up study reported hemorrhage from several previously documented small asymptomatic saccular aneurysms.

Although some authors suggest that the critical size for saccular aneurysm rupture is 4-7 mm in diameter, they also caution that a critical size below which SAH does not occur does not appear to exist. When an aneurysm is discovered incidentally or at the time of investigation of SAH from another source, consider definitive repair of the unruptured lesion because small asymptomatic aneurysms clearly are not innocuous.

Other risk factors, such as age, sex, hypertension, or multiple aneurysms, seem to have comparatively little relationship to the risk of aneurysm rupture.

Flow dynamics and aneurysm growth

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. Wall shear stress caused by the rapid changes of blood flow direction in the aneurysm that occur with systole and diastole produce continuing damage to 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.

Recent studies demonstrate that the geometric relationship between an aneurysm and its parent artery is the principal factor determining intra-aneurysmal flow patterns. In lateral aneurysms, such as those arising 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 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

Some vasculopathies, such as FMD (see Multiplicity), have an increased incidence of cephalocervical aneurysms. Some vasculitides, such as systemic lupus erythematosus (SLE) and even Takayasu arteritis, have been associated with aneurysms. Substance abuse, especially of cocaine, can cause certain forms of vasculitis, thus contributing to aneurysm formation, or can cause hemorrhage from preexisting vascular abnormalities such as AVMs or saccular aneurysms.

Vasculopathies

• SLE: Commonly reported CNS vascular lesions with SLE are 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 (see Images 9-16).

• Takayasu arteritis: The characteristic vascular lesions are occlusion, stenosis, and luminal irregularities, but ectasia and aneurysm formation have been described in Takayasu arteritis.

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

• Drug abuse: Various intracranial vascular lesions have been reported with substance abuse.
  • Cocaine abuse is associated with various CNS complications, including subarachnoid hemorrhage, cerebral ischemia or infarction, intraparenchymal hemorrhage, seizures, vasculitis, vasospasm, and death. Approximately 50% of patients who have a drug abuse problem 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.

Although MRA appears promising, definitive diagnosis and preoperative delineation of intracranial aneurysms are achieved with catheter angiography.

The role of diagnostic cerebral angiography in patients with nontraumatic SAH is to identify the presence of any aneurysms, to delineate the relationship of an aneurysm to its parent vessel and adjacent penetrating branches, to define the potential for collateral circulation to the brain, and to assess for vasospasm.

Technically adequate cerebral angiography is essential in the assessment of nontraumatic SAH. This requires visualizing the entire intracranial circulation, including the anterior and posterior communicating arteries and both posterior inferior cerebellar arteries. Injections with cross-compression, multiple oblique plus submental vertex views and the standard anteroposterior and lateral projections, and subtraction studies (whether cut film or high-resolution digital) are integral parts of the complete angiographic evaluation.

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 usually 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 dilations 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, regular in shape, and the distal vessel exits from their apices.

Vascular loops are caused by overlapping projections of a 3-dimensional vessel onto a 2-dimensional image. Typically, they appear denser than an aneurysm and can be identified using multiple oblique views.

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 on CT scan surrounding an aneurysm is diagnostic of rupture. Larger aneurysms are also more likely to rupture. Lobulation or an irregularly shaped 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.

In approximately 15% of patients with nontraumatic SAH, no aneurysm is found despite a complete, high-quality, 4-vessel cerebral angiogram. Two distinct subsets of these patients have been recognized. The first group consists of those with so-called nonaneurysmal perimesencephalic SAH, in which bleeding on CT scan 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 these patients, and their prognosis is excellent. In these cases, SAH probably results from spontaneous rupture of small pontine or perimesencephalic veins.

In the second group with angiogram-negative SAH, CT scans reveal an aneurysmal pattern of hemorrhage, ie, blood fills the suprasellar cistern and extends completely into the lateral sylvian or anterior interhemispheric fissures. The risk of rebleeding, cerebral ischemia, and neurologic deficit is high in this group and warrants repeat angiography to identify an occult aneurysm. Repeat 4-vessel cerebral angiography demonstrates a lesion in 10-20% of these cases.

Computed tomography scan

Bone erosion can be observed in long-standing lesions that arise near the skull base. Mural calcification is uncommon, with both punctate and curvilinear types identified. The attenuation characteristics of a saccular aneurysm vary, depending on whether the lesion is patent and partially or completely thrombosed.

Patent aneurysms

On noncontrast CT scan, 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 intravenous contrast material. Angiographiclike images of the cerebral vasculature can be obtained using rapid contrast infusion and thin-section dynamic CT scanning. Various 3-dimensional 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, such as giant aneurysms, and delineate their relationships to adjacent structures.

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

Thrombosed aneurysms

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 may appear hypodense on CT scans.

Subarachnoid hemorrhage

The presence of SAH may complicate the CT scan appearance of aneurysms. The reported ability of CT scan to detect SAH caused by ruptured cerebral aneurysms in the acute phase is from 95%. 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 with SAH. However, some bleeding patterns have been associated with particular aneurysm locations.

Hemorrhage located predominantly within the interhemispheric fissure is common with anterior communicating artery aneurysms, and sylvian fissure blood is often observed with MCA lesions. Intraventricular blood can be helpful in localizing ruptured aneurysms. Fourth ventricle hemorrhage is common with posterior fossa aneurysms, and frontal horn blood typically occurs with anterior communicating artery lesions.

Magnetic resonance imaging

Aneurysm appearance 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

Patent aneurysms can produce hyperintense or hypointense signals on routine MRI studies, depending on specific flow characteristics and pulse sequences used. The typical patent aneurysm lumen with rapid flow is visible as a well-delineated suprasellar 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.

Intravenous 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.

Thrombosed aneurysms

Partially thrombosed aneurysms often have a complex signal on MRI scans. 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.

Magnetic resonance angiography

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 maps or MRAs (see Image 11).

Two standard techniques currently used for MRA are 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 that are 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.

Place all patients on calcium channel blockers (nimodipine for 21 d) on admission to prevent and treat vasospasm. Treat all patients aggressively with HHH (hypertension, hypervolemia, hemodilution) therapy if vasospasm is suspected. This remains the most important aspect of the medical management of vasospasm, but, in refractory cases where medical management fails, use endovascular methods with transluminal balloon angioplasty or intra-arterial papaverine.

Blood in the subarachnoid space obliterates the arachnoidal villi and can cause acute hydrocephalus, which can lead to neurologic worsening because of the raised intracranial pressure (ICP). In this situation, place an immediate intraventricular catheter with CSF drainage. Not only can this be lifesaving, but also a patient's neurologic examination can improve dramatically after the hydrocephalus has been treated.

Surgical treatment

See Images 12-13.

Surgical clipping

The goal of surgical treatment is usually to place a clip across the neck of the aneurysm to exclude the aneurysm from the circulation  without occluding normal vessels. When the aneurysm cannot be clipped because of the nature of the aneurysm or poor medical condition of the patient, the following alternatives may be considered:

• Wrapping: Although this 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: Effective treatment requires both distal and proximal arterial interruption by direct surgical means (ligation or occlusion with a clip), by placement of a detachable balloon, or some combination. Treatment also may incorporate extracranial-intracranial (EC-IC) bypass to maintain flow distal to the trapped segment.

• Proximal (hunterian) ligation: Proximal ligation is useful for giant aneurysms. For nongiant aneurysms it provides little benefit and adds to the risk of thromboembolism (which may be reduced by occluding the CCA rather than the ICA). This may elevate the risk of developing aneurysms in the contralateral circulation.

After performing a craniotomy, use microsurgical techniques with the operative microscope to dissect free the aneurysm neck 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 manufactured in various types, shapes, sizes, and lengths and are usually MRI compatible. The operative mortality rate is less than 5% with an experienced physician who uses the operative microscope, microsurgical instrumentation, temporary artery occlusion, modern neuroanesthesiology techniques, and intraoperative micro-Doppler.

Technical approach by artery

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.

Postoperative care

Most agree that an angiogram is necessary after surgery to confirm good clip placement with total obliteration of the aneurysm and patency of the surrounding vessels. In cases where this is accomplished, the rebleeding rate is negligibly low.

After successful obliteration of the aneurysm, the patient remains at significant risk for vasospasm, hydrocephalus, and medical complications and remains in an intensive care setting for at least 7-10 days. Operative complications represent only a small portion of the morbidity and mortality rates associated with a ruptured intracranial aneurysm. The major causes of morbidity and mortality are misdiagnosis, rebleeding, and vasospasm.

Vasospasm is defined as angiographic narrowing that can lead to delayed ischemia. Clinically, vasospasm is diagnosed as deterioration in mental status or focal neurologic deficits, most commonly hemiparesis or dysphasia. Transcranial Doppler frequently is used as a noninvasive diagnostic tool and is sensitive to changes in the vessel caliber of the larger vessels of the circle of Willis. If the patient’s condition deteriorates, excluding all other causes of neurologic deterioration is important. If in doubt, a cerebral angiogram is indicated to confirm the diagnosis. Vasospasm must be aggressively managed once it is detected because it can lead to permanent disability and to death.

Once an intraventricular catheter is placed or if gliosis obliterates the subarachnoid space, permanent communicating hydrocephalus develops in approximately 20% of cases. In such instances, a shunting procedure, usually a ventricular or a lumboperitoneal shunt, is required.

Endovascular surgery

See Images 14-15.

During the past decade, endovascular methods have been developed 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 and colleagues 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. This has proven to be a very valuable technique, and excellent obliteration can be accomplished in accessible aneurysms with small necks. This technique is especially well suited for posterior fossa aneurysms.

The most common coils 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.

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 3-4 times more thrombogenic than stainless steel. The platinum coil is delivered by a stainless steel delivery system, which is detached by electrolysis.

Numerous experimental and human series have indicated that the thrombotic reaction induced by electrothrombosis is not complete. For this reason, modifications of the coil surface are underway 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 receive a lower amount of intravenous heparin bolus to achieve an ACT longer than 200 seconds, with an additional bolus administered after the first coil is delivered within the aneurysm cavity to increase the ACT to longer than 250 seconds.

For each embolization procedure, a 6F guide catheter is placed in the cervical internal carotid or VA. A 0.014-inch microguidewire is navigated into the aneurysm cavity using magnified road-mapping technique.

A microcatheter with 2 radiopaque markers is advanced into the aneurysm cavity. Coils of decreasing sizes are delivered into the aneurysm cavity and electrolytically detached. Angiograms are obtained before detaching each coil 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 placement has been used in such patients.

Choice of surgical technique

Whether to obliterate an aneurysm surgically through a craniotomy and clipping or to use endovascular methods is a decision made by the neurosurgeon and the endovascular radiologists as a team based on which approach best suits each patient's aneurysm. The general consensus today is that treatment depends on the age of the patient and the location of the aneurysm. Younger patients tend to undergo surgical clipping because coiling has a high recurrence rate. Posterior fossa aneurysms (especially the basilar artery tip) tend to be treated using the coil procedure. In most major aneurysm centers, most cases are still obliterated by surgical clipping, but coiling is being used more frequently.

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

• Inflammation and brain edema are most severe immediately following SAH. Such inflammation makes brain retraction more difficult. At the same time, this softens the brain, which also makes retraction more difficult (retractors have a tendency to lacerate the more friable brain).

• The presence of solid clot makes surgery more difficult.

• The risk of intraoperative rupture is higher with early surgery.

• The incidence of vasospasm may be increased following early surgery from mechanotrauma to vessels.

Factors favoring the choice of early surgery include the following:

• Good medical condition of patient

• Good neurologic condition of patient (Hunt and Hess grade <3)

• Large amounts of subarachnoid blood, increasing the likelihood and severity of subsequent vasospasm (clipping the aneurysm facilitates treatment of vasospasm)

• Conditions that complicate management in the face of unclipped aneurysm (eg, unstable blood pressure, frequent and/or intractable seizures)

• Large clot with mass effect associated with SAH

• Early rebleeding, especially multiple rebleeds

• Indications of imminent rebleeding (eg, development of third nerve palsy with posterior communicating artery aneurysm, increase in aneurysm size on repeat angiography)

Factors favoring delayed surgery (10-14 d post-SAH) include the following:

• Poor medical condition of patient

• Poor neurologic condition of patient, ie, Hunt and Hess grade >4, (This is controversial; some say the risk of rebleeding and its mortality rate argues for early surgery even in patients with a high grade.)

• Aneurysms difficult to clip because of large size or difficult location necessitating a lax brain during surgery (eg, difficult basilar bifurcation or midbasilar artery aneurysms, giant aneurysms)

• Significant cerebral edema observed on CT scan

Class 1 data are insufficient to establish any firm conclusions. Therefore, the following discussion is based on trials that are nonrandomized.

Overall, the trend is towards better outcome with early surgery than with later surgery. Outcomes seem worse when surgery is performed 4-10 days after SAH (the "vasospastic interval") than if performed early or late.

A dilemma - To treat or not to treat

Modern diagnostic techniques allow the detection of many potentially dangerous conditions before patients are affected, often before symptoms occur. The ability to detect 4 such conditions, ie, asymptomatic carotid-artery stenosis, atrial fibrillation without brain embolism, vascular malformations in the brain, and cerebral aneurysms, has led to controversy about preventive treatment. All 4 are serious disorders that can cause disabling or fatal brain infarction or hemorrhage.

Treatment of these conditions, which consists of surgery in patients with carotid artery disease, aneurysms, or vascular malformations and anticoagulant therapy in elderly persons with atrial fibrillation, carries considerable risks as well as potential benefits. Physicians are schooled in the tradition of primum non nocere, and many physicians as well as patients endorse the adage, "If it isn’t broken, don't fix it," noting that it is impossible to make a person with an asymptomatic condition feel better. Other doctors, however, think repair of any lesion is warranted. The issues raised are broad, and they hinge on the question of how doctors decide to treat individual patients.

Choosing surgery for patients with unruptured intracranial aneurysms involves weighing the risk of intracranial hemorrhage against the risks associated with brain surgery. In this section, the authors review the studies most pertinent to this issue.

In the International Study of Unruptured Intracranial Aneurysms, investigators retrospectively analyzed the frequency of rupture among 1449 patients with unruptured intracranial aneurysms, some of which were discovered during the treatment of SAH caused by the rupture of other aneurysms.

Size, location, and previous SAH were the most important features that predicted aneurysmal rupture. As in other circumstances, biologic characteristics proved to be very important. Patients with previously ruptured aneurysms had 11 times the rate of rupture of patients without prior hemorrhage. Aneurysm size was prognostically important. Aneurysms smaller than 10 mm in diameter had a very low rate of rupture. Location was also important. Aneurysms at the junction of the internal carotid and posterior communicating arteries and aneurysms within the vertebrobasilar system, especially those at the rostral basilar-artery bifurcation, had a higher rate of rupture than other aneurysms.

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% for patients younger than 45 years, 14.4% for those aged 45-64 years, and 32% for 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 that were smaller than 10 mm in diameter.

Previous studies, performed at the Mayo Clinic, also emphasized size as the main prognostic feature. In a 1981 study of 65 patients with 81 unruptured aneurysms, none of the 44 aneurysms that were 10 mm in diameter or smaller ruptured, as compared with 8 ruptures of 29 aneurysms that were larger than 10 mm. In a 1987 study of 130 patients with 161 unruptured aneurysms, saccular aneurysms that were less than 10 mm in diameter had a very low rate of rupture; the mean diameter of the ruptured aneurysms was 21.3 mm. The mean diameter of ruptured aneurysms at the Mayo Clinic during this period was 7.5 mm. However, other large studies have shown that small aneurysms may cause SAH.

In the Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage, which involved 6038 ruptured aneurysms, the critical size for rupture was 7-10 mm. In another study involving 650 patients with aneurysmal rupture, the average size of ruptured aneurysms was 8 mm. This study is criticized by most neurosurgeons because it included ophthalmic artery aneurysms, which might have biased the data.

Intracranial aneurysms cause symptoms other than clinically recognized subarachnoid hemorrhage. Episodes of minor bleeding, often referred to as sentinel hemorrhages or "warning leaks," occur often and are frequently undetected. Some aneurysms produce pressure on cranial nerves and brain structures, causing headache and neurologic symptoms and signs. Aneurysms can harbor thrombi that embolize distally, causing episodes of brain ischemia.

Prudent physicians must weigh many characteristics in each case. The size and location of the aneurysm and the presence or absence of a history of ruptured aneurysms are important. Consider also the patient's symptoms. Consider surgery in case of major compressive symptoms. Coexisting medical problems are common in patients with aneurysms. Hypertension increases the risk of bleeding. Poorly controlled hypertension, especially in patients known to be noncompliant with treatment, is therefore a factor that favors surgery. The presence of cancer or severe cardiac, pulmonary, or renal disease weighs against prophylactic surgery. Factors related to surgery are also critical. The location of some aneurysms makes surgery particularly difficult and hazardous. The morphologic features of the aneurysm, for example, whether it has a neck that can be clipped, also influence the outcome of surgery. And, of course, some surgeons have better results with respect to morbidity and mortality rates than others.

Many patient-related factors also must be considered. Age is very important. Surgery seems more reasonable in young patients, who face many years at risk, than in older patients. The patient's feelings, experiences, biases, and personal preferences are also important. Many patients do not accept the immediate risk of death or disability associated with surgery to prevent the possibility of rupture at some time in the future. 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.

A decision of whether to treat an unruptured intracranial aneurysm surgically, like many other difficult therapeutic decisions, 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.



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