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Cerebral Aneurysm
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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.
CAUSES AND CLASSIFICATION OF INTRACRANIAL ANEURYSMS
The common causes of intracranial aneurysm are hemodynamic induced/degenerative
vascular injury, atherosclerosis (typically leads to fusiform aneurysms), underlying
vasculopathy (eg, fibromuscular dysplasia), and high-flow states, as in arteriovenous
malformation (AVM) and fistula.
Uncommon causes include trauma, infection, drugs, and neoplasms (primary or
metastatic).
Intracranial aneurysms are classified as follows:
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Saccular aneurysms
o Developmental/degenerative
o Traumatic
o Mycotic
o Oncotic
o Flow-related
o Vasculopathy-related
o Drug-related
Fusiform aneurysms
Dissecting aneurysms
SACCULAR ANEURYSMS
Developmental/degenerative aneurysms
Pathology
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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
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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:
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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.
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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.
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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.
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Subarachnoid hemorrhage
o 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.
o On presentation, patients typically report experiencing the worst headache
of their lives. The association of meningeal signs should increase
suspicion of SAH.
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,
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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 longterm 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 47 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
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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
Traumatic aneurysms account for less than 1% of all aneurysms. Two general types of
traumatic aneurysms are identified, aneurysms secondary to penetrating trauma and
aneurysms secondary to nonpenetrating trauma.
Penetrating trauma
Intracerebral aneurysms secondary to penetrating injuries are commonly due to highvelocity missile wounds of the head. A recent 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 scan
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 scan or magnetic resonance (MR)
studies.
Occasionally, the external carotid artery is a site of traumatic injury. The superficial
temporal artery (STA) is the most commonly affected vessel. STA traumatic
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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 hemorrhage from a
meningeal pseudoaneurysm occurs, it is usually into the epidural space. Direct
penetrating injury to the VA is uncommon. Occasionally, cervical spine fracturedislocations damage the VA. These typically produce dissection or occlusion;
pseudoaneurysms are rare.
Nonpenetrating trauma
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
anterior cerebral artery 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
juxtafalcial hematoma is observed on CT scan.
Suspect traumatic cortical artery aneurysm if a delayed hematoma near the brain
periphery develops adjacent to the site of a skull fracture.
Treatment
Although cases have been reported with spontaneous resolution, direct treatment is
usually recommended. Perform balloon trapping or balloon embolization on ICA
aneurysms at the skull base. Treat peripheral lesions surgically with clipping of the
aneurysm neck, excision of the aneurysm, or wrapping, if no other method is feasible.
Mycotic aneurysms
The term mycotic aneurysm refers to any aneurysm that results from an infectious
process involving 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.
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In the past, mycotic aneurysms were 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.
Treatment
Mycotic aneurysms generally have a fusiform morphology and are usually very friable.
Therefore, surgical treatment is difficult and/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 mo) helps document the effectiveness of medical therapy. Even if aneurysms seem
to be shrinking, they may subsequently increase, and new ones may form.
Serial magnetic resonance angiography (MRA) may be a viable alternative in some
cases. Aneurysms may continue to shrink following completion of antibiotic therapy.
Delayed clipping may be more feasible; indications include patients with SAH,
increasing size of aneurysm while on antibiotics (this is controversial; some argue that
this is not mandatory), and failure of the aneurysm to shrink after 4-6 weeks of
antibiotics. Patients with subacute bacterial endocarditis requiring valve replacement
should have bioprosthetic (ie, tissue) valves instead of mechanical valves to eliminate
the need for risky anticoagulation.
Oncotic aneurysms
Extracranial oncotic pseudoaneurysms with exsanguinating epistaxis are a common
terminal event with malignant head and neck tumors. Intracranial oncotic aneurysms are
less common. Such 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.
Primary tumors
Intracranial aneurysms associated with primary brain tumors are less common than
those caused by metastases. The incidence of saccular aneurysms in patients with
primary cerebral neoplasms does not appear to be significantly higher than the
incidence of aneurysms in the general population, although some authors report a
slightly higher incidence with meningiomas.
Metastatic tumors
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Some metastatic tumors that have been implicated in the development of intracranial
aneurysm are left atrial myxoma and choriocarcinoma. Because metastatic tumors are
common at the gray-white junction, aneurysms from metastatic implants often involve
peripheral cerebral vessels.
Flow-related aneurysms
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
feeding 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 flowweakened 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.
Vasculopathy-, vasculitis-, and drug-related 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
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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.
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Drug abuse: Various intracranial vascular lesions have been reported with
substance abuse.
o 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.
o 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
Pathology
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.
Clinical presentation
Fusiform aneurysms usually occur in older patients. The vertebrobasilar system is
commonly affected. Fusiform aneurysms may thrombose, producing brainstem
infarction. They can also compress the adjacent brain or cause cranial nerve palsies.
Imaging
Fusiform atherosclerotic aneurysms usually arise from elongated tortuous arteries.
Patent aneurysms enhance strongly after contrast administration; thrombosed
aneurysms are hyperintense on noncontrast CT scans. Tubular calcification with
intraluminal and mural thrombi in the ectatic parent vessels and aneurysm wall is
frequent. Occasionally, fusiform aneurysms cause erosion of the skull base.
At 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 relationship between
vessels and adjacent structures such as the brainstem and cranial nerves.
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DISSECTING ANEURYSMS
Pathology
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. 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.
Etiology
Dissecting aneurysms may arise spontaneously. More commonly, trauma or an
underlying vasculopathy such as FMD is implicated.
Location
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.
Imaging
Dissecting aneurysms are elongated, ovoid, or saccular contrast collections that extend
beyond the vessel lumen. 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.
IMAGING OF INTRACRANIAL ANEURYSMS
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Angiography
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.
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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 welldelineated 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,
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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
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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.
A recently developed multislab 3-dimensional TOF technique, multiple overlapping thinsection acquisition (MOTSA), combines the advantages of 2-dimensional multiple
section and direct 3-dimensional 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.
MANAGEMENT OF INTRACRANIAL ANEURYSMS
This section highlights the basic principles of aneurysm treatment. Management of SAH
is discussed in Subarachnoid Hemorrhage.
After an aneurysm is demonstrated arteriographically, the neurosurgeon must decide
how and when to obliterate the aneurysm. In the earlier days of aneurysm treatment,
surgery was delayed until the second or third week after the initial hemorrhage to avoid
difficulty related to a swollen brain during surgery. Although this lowered surgical
morbidity and mortality rates, management results were not always good because of a
high incidence of rebleeding and difficulty in managing vasospasm. For this reason,
most authorities advocate early surgical intervention within the first 48 hours after
hemorrhage, especially in patients with good neurological grade.
Initial evaluation
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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:
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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
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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.
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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.
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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.
TIMING OF TREATMENT
Early versus late surgery
Controversy exists between so-called early surgery (generally, but not precisely defined
as 48-96 h post-SAH) and late surgery (usually >10-14 d post-SAH).
Early surgery is advocated for the following reasons:
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If successful, surgery virtually eliminates the risk of rebleeding, which occurs
most frequently in the period immediately following SAH.
Early surgery facilitates treatment of vasospasm, which peaks in incidence
between days 6 and 8 after SAH (never observed before day 3) by allowing
induction of arterial hypertension and volume expansion without danger of
aneurysmal rupture.
Surgery allows lavage to remove potentially vasospasmogenic agents from
contact with vessels (including use of thrombolytic agents .
Although the operative mortality rate is higher (this finding is controversial), the
overall patient mortality rate is lower.
Arguments against early surgery and in favor of late surgery include the following:
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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.
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Factors favoring the choice of early surgery include the following:
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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:

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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
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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
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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.
REFERNECES:

Berenstein A, Flamm ES, Kupersmith MJ: Unruptured intracranial aneurysms. N
Engl J Med 1999 May 6; 340(18): 1439-40; discussion 1441-2
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Biousse V, Newman NJ: Aneurysms and subarachnoid hemorrhage. Neurosurg
Clin N Am 1999 Oct; 10(4): 631-51
Flamm ES, Grigorian AA, Marcovici A: Multifactorial analysis of surgical outcome
in patients with unruptured middle cerebral artery aneurysms. Ann Surg 2000
Oct; 232(4): 570-5
Goldman: Cecil Textbook of Medicine. 21st ed. Philadelphia, Pa: W B Saunders
Co; 1999.
Greenberg MS: Handbook of Neurosurgery. 4th ed. Lakeland, Fl: Theme Medical
Pub; 1997
Hunt WE, Hess RM: Risks and benefits of screening for intracranial aneurysms in
first-degree relatives of patients with sporadic subarachnoid hemorrhage . 1969;
341(18): 1344.
Johnston SC, Wilson CB, Halbach VV, et al: Endovascular and surgical
treatment of unruptured cerebral aneurysms: comparison of risks. Ann Neurol
2000 Jul; 48(1): 11-9
Kappelle LJ, Eliasziw M, Fox AJ: Small, unruptured intracranial aneurysms and
management of symptomatic carotid artery stenosis. North American
Symptomatic Carotid Endarterectomy Trial Group. Neurology 2000 Jul 25; 55(2):
307-9
Kremer C, Groden C, Hansen HC: Outcome after endovascular treatment of
Hunt and Hess grade IV or V aneurysms: comparison of anterior versus posterior
circulation. Stroke 1999 Dec; 30(12): 2617-22
Morey SS: AHA recommendations for the management of intracranial
aneurysms. Agency for Health Care Policy and Research. Am Fam Physician
2001 Jun 15; 63(12): 2465-6
Newell DW, Elliott JP, Eskridge JM: Endovascular therapy for aneurysmal
vasospasm. Crit Care Clin 1999 Oct; 15(4): 685-99, v
Olafsson E, Hauser WA, Gudmundsson G: A population-based study of
prognosis of ruptured cerebral aneurysm: mortality and recurrence of
subarachnoid hemorrhage. Neurology 1997 May; 48(5): 1191-5
Raaymakers TW, Rinkel GJ, Ramos LM: Initial and follow-up screening for
aneurysms in families with familial subarachnoid hemorrhage. Neurology 1998
Oct; 51(4): 1125-30
Raaymakers TW: Aneurysms in relatives of patients with subarachnoid
hemorrhage: frequency and risk factors. MARS Study Group. Magnetic
Resonance Angiography in Relatives of patients with Subarachnoid hemorrhage.
Neurology 1999 Sep 22; 53(5): 982-8
Speth CP: Risks and benefits of screening for intracranial aneurysms. N Engl J
Med 2000 Mar 9; 342(10): 739-40
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Florida Heart CPR*
Cerebral Aneurysm Assessment
1. Aneurysm is an abnormal local dilatation in the wall of a blood vessel, usually an
artery, due to:
a. Disease
b. Defect
c. Injury
d. All of the above
2. The three types of intracranial aneurysms are:
a. Oncotic, fusiform, and flow related
b. Traumatic, mycotic, and saccular
c. Saccular, fusiform and dissecting
d. Traumatic, mycotic, and dissecting
3. The aneurysmal sac itself is usually composed only of:
a. Intima and adventitia
b. Intima and tunica media
c. Tunica media and adventitia
d. Intima only
4. In the past, most saccular or intracranial berry aneurysms were thought to be
congenital in origin. However, recent studies have found scant evidence for
congenital, developmental, or inherited weakness of the arterial wall. Most
intracranial aneurysms probably result from hemodynamically induced
a. Lipidemia
b. Vascular injury
c. Anemia
d. Hypotension
5. Aneurysms typically become symptomatic in people aged _____ years.
a. 30-50
b. 40-60
c. 50-70
d. 18 and over
6. Aneurysms commonly arise at the bifurcations of _______.
a. Major arteries
b. Major veins
c. Arterioles
d. Venules
7. Approximately 85% of all intracranial aneurysms arise on the
a. anterior (carotid) circulation
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b. posterior circulation
c. basilar artery bifurcation
d. pericallosal artery origin
8. Most intracranial aneurysms
a. Do not cause symptoms until they rupture
b. Do not cause symptoms when they rupture
c. Are not painful when they rupture
d. Do not cause headaches when they rupture
9. Definitive diagnosis and preoperative delineation of intracranial aneurysms are
achieved with
a. An x- ray
b. Catheter angiography
c. A PET scan
d. A CT scan
10. The most important features that predicted aneurysmal rupture are:
a. Size
b. Location
c. Previous subarachnoid hemorrhage
d. All of the above
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