Aneurysm

10/4/21, 9:12 PM https://emedicine.medscape.com/article/1161518-print
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emedicine.medscape.com

Cerebral Aneurysms
Updated: Dec 06, 2018
Author: David S Liebeskind, MD, FAAN, FAHA, FANA; Chief Editor: Helmi L Lutsep, MD
Overview
Practice Essentials
A consequence of cerebral aneurysm, aneurysmal subarachnoid hemorrhage (SAH) has devastating consequences. About 10%
of individuals with aneurysmal SAH die before reaching medical attention, 25% die within 24 hours, and 40-49% die within 3
months. Mortality has been estimated to be as high as 65%, with most deaths occurring early in the clinical course. See the
image below.
Signs and symptoms
Symptoms associated with cerebral aneurysms and SAH are as follows:
Headache
Facial pain
Alterations in consciousness
Seizures
Manifestations of meningeal irritation
Autonomic disturbances
Focal neurologic complaints
Visual symptoms
Respiratory dysfunction
Cardiovascular instability
Hormonal dysfunction
Epistaxis
Specific physical examination findings may include prominent scalp veins, signs of congestive heart failure (eg, vein of Galen
aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).
Neurologic findings exhibit considerable variability because of differences in aneurysm characteristics. These findings include
the following:
Aneurysmal SAH: May be accompanied by nuchal rigidity, decreased level of consciousness, subhyaloid hemorrhages,
pupillary abnormalities (ie, typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits
Giant aneurysms or dolichoectatic aneurysms: May cause mass effects and distal thromboembolism with prominent focal
deficits; these aneurysms may also result in optic atrophy or other cranial neuropathies or cause brainstem compression.
Specific syndromes have been associated with particular aneurysmal locations. For example, aneurysms at the anterior
communicating artery, the most common site of aneurysmal SAH (34%), have the following characteristics:
These aneurysms are usually silent until they rupture

Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or
hypothalamic dysfunction.
Neurologic deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage
(63%), acute hydrocephalus (25%), or frontal lobe strokes (20%)
See Clinical Presentation for more detail.
Diagnosis
Lab studies used in the diagnosis and assessment of cerebral aneurysms include the following:
Complete blood count (CBC) with platelets: Monitor for infection, evaluate anemia, and identify bleeding risk
Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy that increases bleeding risk
Serum chemistries, including electrolytes and osmolarity: Obtain baseline studies to monitor hyponatremia, address
arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial
pressure
Liver function tests: Identify hepatic dysfunction that may complicate clinical course
Arterial blood gases: Assess blood oxygenation
Imaging studies used in the workup of cerebral aneurysms include the following:
Computed tomography (CT) scanning: Aneurysmal SAH may be detected in 90-95% of cases
Magnetic resonance imaging (MRI): Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH,
although the comparison of CT scanning with MRI in the detection of SAH is controversial; dolichoectatic and giant
aneurysms are identified readily with MRI
Angiography: Conventional angiography is the definitive procedure for the detection and characterization of cerebral
aneurysms
Transcranial Doppler ultrasonography: This modality facilitates the diagnosis of vasospasm and serial monitoring of
cerebral blood flow at the bedside
Single-photon emission CT (SPECT) scanning, positron emission tomography (PET) scanning, xenon-CT (XeCT)
scanning: With these techniques, cerebral blood flow studies may depict ischemia associated with vasospasm, although
these modalities are not routinely employed
Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with
an unwitnessed loss of consciousness
Echocardiography: Cardiac sources of embolism, including endocarditis and myxomas, may be visualized in cases of
infectious or neoplastic aneurysms.
Lumbar puncture may help establish the diagnosis of SAH in the absence of focal signs of mass effects. Aneurysmal
SAH demonstrates hemorrhagic cerebrospinal fluid with a xanthochromic supernatant, although these findings may be
absent within the first few hours following aneurysmal rupture.
See Workup for more detail.
Management
Nonsurgical therapy
Medical treatment of cerebral aneurysms involves general supportive measures and prevention of complications for individuals
who are in the periprocedural period or are poor surgical candidates.
Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel
blockers, and prevention of seizures.
Surgical treatment
Microsurgical techniques focus on exclusion of the aneurysm from the cerebral circulation and reduction of mass effects on
adjacent structures. A surgical clip usually is placed across the aneurysm neck with preservation of the parent vessel,

eliminating any aneurysmal rests that may subsequently redevelop.
Endovascular treatment
Endovascular coiling of cerebral aneurysms has been found to yield a better clinical outcome than clipping does, with the benefit
greatest in patients with a good preoperative grade.[1, 2]
See Treatment and Medication for more detail.
Background
Cerebral aneurysms are pathologic focal dilatations of the cerebrovasculature that are prone to rupture. These vascular
abnormalities are classified by presumed pathogenesis. Saccular, berry, or congenital aneurysms constitute 90% of all cerebral
aneurysms and are located at the major branch points of large arteries. Dolichoectatic, fusiform, or arteriosclerotic aneurysms
are elongated outpouchings of proximal arteries that account for 7% of all cerebral aneurysms. Infectious or mycotic aneurysms
are situated peripherally and comprise 0.5% of all cerebral aneurysms. Other peripheral lesions include neoplastic aneurysms,
rare sequelae of embolized tumor fragments, and traumatic aneurysms. Traumatic injury also may result in dissecting
aneurysms in proximal vessels. Microaneurysms of small perforating vessels may result from hypertension.
Saccular aneurysms are situated in the anterior circulation in 85-95% of cases, whereas dolichoectatic aneurysms affect
predominantly the vertebrobasilar system. The location of saccular aneurysms at specific arterial segments varies in frequency
because of differences in reported study populations. Multiple saccular aneurysms are noted in 20-30% of patients with cerebral
aneurysms.
Saccular aneurysms frequently rupture into the subarachnoid space, accounting for 70-80% of spontaneous subarachnoid
hemorrhages (SAH). Aneurysmal rupture also may result in intraparenchymal, intraventricular, or subdural hemorrhage. Giant
saccular aneurysms, defined as greater than 25 mm in diameter, represent 3-5% of all intracranial aneurysms. Although giant
aneurysms may cause SAH, these lesions frequently produce mass effects and result in distal thromboembolism.
Aneurysmal SAH is a catastrophic condition, affecting 30,000 individuals in the United States every year. Most of these
individuals (60%) either die or suffer permanent disability; 50% of survivors with favorable outcomes experience considerable
neuropsychological dysfunction. Cerebral vasospasm (ie, narrowing of proximal arterial segments) complicates 20-50% of cases
and is the major cause of death and disability associated with aneurysmal SAH.
Pathophysiology
The pathogenesis of cerebral aneurysms is related inherently to structural aberrations of the cerebrovasculature, although the
etiology of these abnormalities may be diverse. The integrity of the internal elastic lamina is compromised, with associated
elastic defects in the adjacent layers of the tunica media and adventitia. Muscular defects of the tunica media and minimal
support of adjacent brain parenchyma augment the pathologic potential of chronic hemodynamic stress on the arterial wall.
Focal turbulence and discontinuity of the normal architecture at vessel bifurcations may account for the propensity of saccular
aneurysm formation at these locations. Distal aneurysms may be smaller compared with proximal sites, yet the risk of rupture
may be dissimilar due to the relatively thinner parent artery wall thickness.
The development of cerebral aneurysms remains a controversial topic. A multifactorial etiology is most likely, reflecting the
interaction of environmental factors, such as atherosclerosis or hypertension, and a congenital predisposition associated with
various vascular abnormalities. Abnormalities of the internal elastic lamina may be congenital or degenerative. Multiple
conditions have been associated with cerebral aneurysms; they include the following:
Autosomal dominant inherited polycystic kidney disease
Fibromuscular dysplasia
Arteriovenous malformations
Osler-Weber-Rendu syndrome
Coarctation of the aorta
Other vascular anomalies

Moyamoya syndrome
Marfan syndrome
Ehlers-Danlos syndrome, type IV
Other collagen type III disorders
Pseudoxanthoma elasticum
Alpha1-antitrypsin deficiency
Systemic lupus erythematosus
Sickle cell anemia
Bacterial endocarditis
Fungal infections
Neurofibromatosis type 1
Tuberous sclerosis
Environmental stressors, such as hypertension, have been associated with the presence of multiple aneurysms. A familial
inheritance pattern has been noted in fewer than 2% of intracranial aneurysms.
Dolichoectatic aneurysms of proximal vessels most likely have an arteriosclerotic etiology. These tortuous, elongated dilatations
devoid of a true aneurysmal neck frequently contain laminated thrombus. Although aneurysmal SAH may occur, these lesions
typically exert mass effects on adjacent parenchyma, with brainstem compression and cranial neuropathies, or result in
obstruction of cerebrospinal fluid (CSF) outflow or distal thromboembolic sequelae.
Infectious aneurysms typically are situated in distal branches of the middle cerebral artery (MCA; 75-80% of cases), reflecting
the embolic origin of these lesions. Cardioembolism of septic material complicates the course of 4% of patients with subacute
bacterial endocarditis and may affect other patients with congenital heart disease and right-to-left shunts. Direct extension from
lumen to adventitia of septic emboli containing Streptococcus viridans or Staphylococcus aureus (ie, the most common
pathogens) may lead to degradation and aneurysm formation. Alternatively, diffuse infiltration from the periphery to the lumen
may occur in the setting of meningitis, exemplified by aneurysms of the basal circulation associated with fungal infections.
Infectious aneurysms are frequently multiple (20%) and have a greater propensity to bleed than other aneurysms.
Traumatic aneurysms may be located in peripheral cortical branches secondary to contact with the falcine edge or skull
fractures associated with penetrating or closed head injury. Traumatic dissecting aneurysms due to expansion of intramural
hematomas are noted most commonly at the skull base. These false aneurysms, devoid of all layers of the vessel wall, may
compress cranial nerves or lead to distal embolization. Rupture of the internal carotid artery (ICA) may produce a carotid-
cavernous fistula.
Distal embolization of tumor fragments from a cardiac myxoma or choriocarcinoma may lead to neoplastic aneurysm formation.
Vein of Galen aneurysms or malformations may cause hydrocephalus associated with aqueductal compromise or congestive
heart failure in infants.
Aneurysmal rupture typically results in SAH, with diffuse or focal forms of vasospasm that may lead to ischemia and infarction.
Recent animal data suggest therapeutic benefit of nitrite infusions to enhance cerebral perfusion in the setting of aneurysmal
SAH. This delayed complication of vasospasm is of unclear pathogenesis but most likely is due to the presence of blood and the
formation of multiple substances in the subarachnoid space. Spontaneous thrombosis of an aneurysm and subsequent
recurrence have been reported in a few cases.
Frequency
United States
The frequency of cerebral aneurysms is difficult to ascertain because of variation in the definitions of the size of aneurysm and
modes of detection. Autopsy series cite prevalences of 0.2-7.9%. Prevalence ranges from 5-10%, with unruptured aneurysms
accounting for 50% of all aneurysms. Pediatric aneurysms account for only 2% of all cerebral aneurysms. In the United States,

the incidence of ruptured aneurysms is approximately 12 per 100,000 individuals or 30,000 annual cases of aneurysmal SAH.
The frequency of cerebral aneurysms has not declined in recent years.
International
Incidence of aneurysmal SAH varies widely depending on geographic location, ranging from 3.9-19.4 per 100,000 individuals,
with the highest reported rates in Finland and Japan. Overall, the incidence has been estimated at 10.5 per 100,000 individuals.
Mortality/Morbidity
Aneurysmal SAH has devastating consequences. About 10% of individuals with aneurysmal SAH die before reaching medical
attention, 25% die within 24 hours, and 40-49% die within 3 months. Mortality rate has been estimated to be as high as 65%,
with most deaths occurring early in the clinical course.
Early surgical treatment is associated with higher operative morbidity and mortality rates; however, overall morbidity and
mortality rates are lower in patients who undergo surgery. Intraoperative aneurysmal rupture has a combined morbidity and
mortality rate of 30-35%.
Aneurysmal SAH during pregnancy has a mortality rate of 35%, accounting for one of the leading causes of maternal mortality
during pregnancy.
In one study of 102 pediatric patients with cerebral aneurysm followed for a mean of 26.8 years, researchers found long-term
excess mortality after successful treatment of ruptured aneurysms, especially among males; this excess mortality was largely
aneurysm-related.[3]
Race
The racial predilection of cerebral aneurysms is largely unknown, although a higher incidence has been noted in African
Americans, with an odds ratio of 2:1.
Sex
Cerebral aneurysms affect equal numbers of women and men younger than 40 years, although women are affected more
frequently in older age groups. Overall, the female-to-male ratio has been estimated at 1.6:1.
Saccular aneurysms are most common in the anterior communicating artery (ACoA) or anterior cerebral artery (ACA) in
men, whereas the junction of the ICA with the posterior communicating artery (PCoA) is the most common site for
saccular aneurysms in women.
Giant aneurysms are 3 times more common in women than men.
The prognosis of aneurysmal SAH is worse for women than men.
Age
See the list below:
Cerebral aneurysms are rarely apparent in infants and children. Clinical manifestations increase with age, reaching a
peak in people aged 55-60 years.
Carotid artery is affected most commonly in individuals younger than 18 years.
The prognosis of aneurysmal SAH worsens with increasing age.

Presentation
History

The clinical presentation of cerebral aneurysms includes symptoms associated with major aneurysmal rupture (eg, SAH), minor
aneurysmal hemorrhage (eg, warning leak or sentinel bleed), nonhemorrhagic manifestations (eg, mass effects or cerebral
ischemia), and asymptomatic scenarios (eg, incidental aneurysm detection or identification through screening[4] ).
Although aneurysmal SAH has characteristic historical features, the constellation of symptoms may vary with location, size,
shape, and direction of the aneurysm.
Aneurysmal rupture also may present with intraparenchymal hemorrhage (more common with distal aneurysms), intraventricular
hemorrhage (13-28%), or subdural hematoma (2-5%).
Minor aneurysmal hemorrhage may precede rupture with a wide variation in latency, although these warning leaks also may be
clinically silent.
Giant aneurysms may compress brain parenchyma, resulting in focal neurological complaints.
Aneurysmal expansion may produce pain or herald new neurological manifestations.
Traumatic aneurysms may have a delayed presentation, with intracranial hemorrhage or recurrent epistaxis.
Symptoms associated with cerebral aneurysms and SAH are as follows:
Headache: This is characterized by the acute onset of severe pain, which patients often describe as "the worst headache
of my life." Aneurysmal expansion, thrombosis, or intramural hemorrhage may cause a subacute, unilateral, periorbital
headache. Headache does not always accompany aneurysmal SAH.
Facial pain: Cavernous-carotid aneurysms may produce facial pain.
Alterations in consciousness: The sudden elevation of intracranial pressure associated with aneurysmal rupture may lead
to a precipitous decline in cerebral perfusion pressure, causing syncope (50% of cases). Confusion or mild impairment in
alertness also may be noted.
Seizures: Focal or generalized seizures are present in 25% of aneurysmal SAH cases, with most events occurring within
24 hours of onset.
Manifestations of meningeal irritation: Neck pain or stiffness, photophobia, sonophobia, or other hyperesthesia may be
noted with SAH.
Autonomic disturbances: Subarachnoid accumulation of products of blood degradation may elicit fever. Nausea or
vomiting, sweating, chills, and cardiac arrhythmias also may be present.
Focal neurological complaints: Hemorrhage or ischemia may manifest with focal deficits including weakness,
hemisensory loss, language disturbances, neglect, memory loss, or olfactory disturbances. Focal symptoms are more
common with giant aneurysms.
Visual symptoms: Blurring of vision, diplopia, or visual field defects may be present.
Respiratory dysfunction or cardiovascular instability: These are ominous signs of brainstem compression.
Hormonal dysfunction: Intrasellar aneurysms may interfere with pituitary function.
Epistaxis: This is noted occasionally with traumatic aneurysms.
Physical
The general examination occasionally reveals manifestations of associated conditions such as subacute bacterial endocarditis,
trauma, or collagen-vascular disease.
Specific physical examination findings may include prominent scalp veins, signs of congestive heart failure (eg, vein of Galen
aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).
Neurologic findings exhibit considerable variability, depending on aneurysm characteristics.
Aneurysmal SAH may be accompanied by nuchal rigidity, decreased level of consciousness, subhyaloid hemorrhages,
pupillary abnormalities (ie, typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits.

Giant aneurysms or dolichoectatic aneurysms may cause mass effects or distal thromboembolism with prominent focal
deficits, optic atrophy or other cranial neuropathies, or brainstem compression.
Specific syndromes have been associated with particular aneurysmal locations.
Anterior communicating artery: This is the most common site of aneurysmal SAH (34%). Usually, ACoA aneurysms are
silent until they rupture. Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism,
amnestic syndromes, or hypothalamic dysfunction. Neurological deficits in aneurysmal rupture may reflect intraventricular
hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%).
Anterior cerebral artery: Aneurysms of this vessel, excluding ACoA, account for about 5% of all cerebral aneurysms.
Most are asymptomatic until they rupture, although frontal lobe syndromes, anosmia, or motor deficits may be noted.
Middle cerebral artery: Aneurysms of the middle cerebral artery, as shown below in the image and video, account for
about 20% of aneurysms, typically at first or second division in the sylvian fissure. Aphasia, hemiparesis, hemisensory
loss, anosognosia, or visual field defects may be noted.
Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.
Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.
Posterior communicating artery: Aneurysms present at the junction of the termination of the ICA and PCoA account for
23% of cerebral aneurysms; they are directed laterally, posteriorly, and inferiorly. Pupillary dilatation, ophthalmoplegia,
ptosis, mydriasis, and hemiparesis may result.
Internal carotid artery: Besides PCoA aneurysms, aneurysms of the ICA, shown below, account for about 4% of all
cerebral aneurysms. Supraclinoid aneurysms may cause ophthalmoplegia due to compression of cranial nerve (CN) III or
variable visual defects and optic atrophy due to compression of the optic nerve. Chiasmal compression may produce
bilateral temporal hemianopsia. Hypopituitarism or anosmia may be seen with giant aneurysms. Cavernous-carotid
aneurysms exert mass effects within the cavernous sinus, producing ophthalmoplegia and facial sensory loss. Rupture of
these aneurysms typically produces a carotid-cavernous fistula, SAH, or epistaxis.

Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.
Basilar artery: Basilar tip aneurysms, shown in the image and the video below, are the most common in the posterior
circulation, accounting for 5% of all aneurysms. Clinical findings usually are those associated with SAH, although
bitemporal hemianopsia or an oculomotor palsy may occur. Dolichoectatic aneurysms may cause bulbar dysfunction,
respiratory difficulties, or neurogenic pulmonary edema.
Cerebral aneurysms. Basilar tip aneurysm illustrated on CT scan (left) and T2-weighted MRI (right).
Cerebral aneurysms. Volume-rendered CT angiography of a basilar tip aneurysm.
Vertebral artery or posterior inferior cerebellar artery: Aneurysms at these arterial segments typically result in ataxia,
bulbar dysfunction, or spinal involvement.
False localizing signs: False localization may be associated with CN III palsy and hemiparesis in uncal herniation, CN VI
palsy with elevated intracranial pressure, homonymous hemianopsia due to posterior cerebral artery compression along
the tentorial edge, brainstem dysfunction associated with tonsillar herniation, and vasospasm in remote vessels.
Causes

See the list below:
Congenital or familial inheritance
Atherosclerosis
Hypertension
Autosomal dominant inherited polycystic kidney disease
Vasculopathies
Arteriovenous malformations, shown below
Cerebral aneurysms. Aneurysm associated with an arteriovenous malformation (AVM) shown on T1-weighted MRI
(left), 3D-time-of-flight MRI (middle), and conventional angiography (right).
Connective tissue disorders
Sickle cell anemia
Infections
Trauma
Neoplasms
Cigarette smoking
Illicit drug use
Alcohol

DDx
Differential Diagnoses
Acute Management of Stroke
Acute Subdural Hematoma in the ED
Anisocoria
Anterior Circulation Stroke
Aphasia
Apraxia and Related Syndromes
Basilar Artery Thrombosis
Cardioembolic Stroke
Carotid Ultrasound
Cavernous Sinus Syndromes

Cerebellar Hemorrhage
Cerebral Venous Thrombosis
Clinical Utility of Evoked Potentials
Cluster Headache
Dermatologic Manifestations of Tuberous Sclerosis
Determination of Brain Death in Children
Dissection Syndromes
Dizziness, Vertigo, and Imbalance
Emergent Management of Subarachnoid Hemorrhage
Fibromuscular Dysplasia
Generalized Tonic-Clonic Seizures
Head Injury
Hydrocephalus
Intracranial Hemorrhage
Intraoperative Neurophysiological Monitoring
Lumbar Puncture (CSF Examination)
Magnetic Resonance Imaging in Acute Stroke
Migraine Headache
Moyamoya Disease
Neurofibromatosis Type 1
Neurological Sequelae of Infectious Endocarditis
Pituitary Tumors
Posterior Cerebral Artery Stroke
Stroke Anticoagulation and Prophylaxis
Stroke Team Creation and Primary Stroke Center Certification
Syncope
Systemic Lupus Erythematosus (SLE)
Thrombolytic Therapy in Stroke
Trigeminal Neuralgia
Vascular Surgery for Arteriovenous Malformations
Vein of Galen Malformation
Workup

Workup

Laboratory Studies
Lab studies that may be helpful for diagnosis include the following:
CBC with platelets: Monitor for infection, evaluate anemia, and identify bleeding risk.
Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy that increases bleeding risk.
Serum chemistries, including electrolytes and osmolarity: Obtain baseline studies to monitor hyponatremia, address
arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial
pressure.
Liver function tests: Identify hepatic dysfunction that may complicate clinical course.
Arterial blood gases: Assess blood oxygenation.
Imaging Studies
Advances in neuroimaging techniques have altered the diagnosis of cerebral aneurysms dramatically. Noninvasive angiographic
methods, such as computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), allow for detection
and characterization of aneurysms, further enhanced by postprocessing techniques that enable 3-dimensional evaluation of
aneurysm morphology. Contemporaneous parenchymal imaging with CT scan or MRI yields a wealth of information that may
assist surgical planning. However, minor aneurysmal hemorrhage may not be detected with noninvasive methods.
A study of 20 years of screening results of individuals with a positive family history of SAH found that the yield of long-term
screening is substantial even after more than 10 years of follow-up and two initial negative screens. These data suggest that
repeated screening should be considered in individuals with 2 or more first-degree relatives who had SAH or unruptured
intracranial aneurysms.[5, 6]
CT scan
Aneurysmal SAH may be detected in 90-95% of cases. If CT scan result is negative and SAH is suspected, perform lumbar
puncture (LP).
Noncontrast CT scan should be performed, as contrast may obscure detection of SAH.
Curvilinear calcification, aneurysmal thrombosis, or bone erosion may be characterized; however, bone structures also may
produce artifacts.
Surrounding edema and an inflammatory reaction may be appreciated with contrast administration following the noncontrast
study.
CTA may detect aneurysms greater than 3 mm, providing detailed evaluation of morphology such as relationship to the parent
vessel and neck width.
CTA can detect more than 95% of aneurysms identified on conventional angiography. CTA may be superior to MRA because of
shorter acquisition times, diminished motion artifacts, and detailed demonstration of other landmarks. However, bone and
venous structures may complicate analysis.
Increasing use of CT perfusion in combination with CTA allows for reconstruction of multiphase CT angiographic images,
potentially providing greater definition beyond standard CTA.[7]
MRI
Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scan and
MRI in detection of SAH is controversial.
MRI may be impractical for patients in unstable condition. Flow voids may be seen extending from the parent vessel into the
aneurysm.
Heterogeneous signal intensity adjacent to the aneurysm wall may be seen with thrombus of varying ages, although MRI is
relatively insensitive to the presence of calcium.

Dolichoectatic and giant aneurysms are identified readily with MRI. Pulsation artifacts and the presence of turbulence may help
to differentiate these aneurysms from other mass lesions, but slow and turbulent flow may preclude visualization on MRA.
MRA may reliably provide 3-dimensional imaging of aneurysms 4 mm or larger.
Phase-contrast techniques may facilitate detection of flow patterns and slow flow. Although phase-contrast MRA is preferable for
large aneurysms, 3-dimensional time-of-flight techniques are preferable for small aneurysms. Source images should be
inspected routinely in conjunction with the reconstructed views.
Angiography
Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms. Aneurysm
location, size, and morphology may be evaluated in the acute or chronic setting with this modality.
Digital subtraction angiography with biplanar magnification views provides details that may be helpful in identifying an acutely
ruptured aneurysm.
Aneurysmal irregularity, the presence of a daughter loculus, or focal spasm may be noted with acute rupture. Vasospasm may
be depicted reliably and the collateral circulation may be demonstrated.
Perform 4-vessel angiography to identify remote vasospasm and the presence of multiple aneurysms. Acute angiography
occasionally yields negative results (eg, due to thrombosis or vasospasm), in which case angiography should be repeated 1-3
weeks later. However, the risk and expense of this procedure may not be appropriate for screening of high-risk individuals.
A junctional dilatation of the terminal carotid artery at the origin of the PCoA may be noted in about 5-10% of patients. These
infundibula or conical enlargements of less than 3 mm are unlikely to enlarge or rupture. However, overt aneurysms at the
juncture of the terminal carotid artery with a persistent PCoA configuration may be more prone to rupture.
Further refinements in the characterization of cerebral aneurysms are expected following the recent introduction of 3-
dimensional rotational angiography. Recent work has demonstrated that this technique may offer superior resolution and
increased sensitivity for detection of small aneurysms.[8]
Other imaging studies
Transcranial Doppler ultrasonography: TCD facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow
at the bedside. TCD has exhibited close correlation with angiography in the setting of vasospasm, typically manifesting 3-21
days following aneurysmal SAH.
Single-photon emission computed tomography (SPECT), positron emission tomography (PET), xenon-CT (XeCT): With these
techniques, cerebral blood flow studies may depict ischemia associated with vasospasm, although these modalities are not
employed routinely.
Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with an
unwitnessed loss of consciousness.
Other Tests
Other tests that may be helpful for diagnosis include the following:
ECG: Cardiac arrhythmias and myocardial ischemia may be evident. Aneurysmal SAH may be associated with several
ECG changes, including peaked P waves, prolonged QT interval, and tall T waves.
Echocardiography: Cardiac sources of embolism, including endocarditis and myxomas, may be visualized in cases of
infectious or neoplastic aneurysms.
Evoked potentials and EEG: These functional neurophysiologic studies may be used to monitor cerebral aneurysm
surgery or patients critically ill with aneurysmal SAH.
Procedures

Lumbar puncture
LP may help to establish the diagnosis of SAH in the absence of focal signs of mass effects. Aneurysmal SAH demonstrates
hemorrhagic CSF with a xanthochromic supernatant, although these findings may be absent within the first few hours following
aneurysmal rupture.
The opening pressure may be elevated.
WBC count may increase after a delay, reflecting a meningeal inflammatory reaction.
The protein may be elevated with normal or decreased glucose.
Cultures may reveal an infectious etiology.
Ventriculostomy: External drainage of CSF may assist in the management of hydrocephalus and cases with poor clinical grades.
Histologic Findings
Gross pathologic examination may reveal brownish pigmentation and fibrous adhesions of surrounding brain parenchyma.
Aneurysm size may be diminished on postmortem examination, although a multilobular shape may be appreciated. A ruptured
fundus may be visualized with calcifications of the aneurysm wall and intraluminal thrombus.
Microscopic examination reveals defects in the normal architecture of the vessel wall. The tunica media and internal
elastic lamina may be absent or degenerated, with hemosiderin-laden phagocytes and lymphocytic infiltration.
Infectious aneurysms may exhibit an infected embolus adherent to a necrotic arterial wall. The intima and internal elastic
lamina may be destroyed with an inflammatory infiltrate consisting of polymorphonuclear cells, lymphocytes, and
macrophages.
Myofilament fragmentation and sarcolemmal destruction may be seen with vasospastic vessels.
Staging
Table 1. Clinical Condition at Presentation (Open Table in a new window)
Grade Clinical Condition at Presentation
0 Unruptured aneurysm
1 Asymptomatic or minimal headache and slight nuchal rigidity
2 Moderately severe or severe headache and nuchal rigidity; cranial neuropathy, no focal deficit
3 Drowsiness, confusion, or mild focal deficit
4 Stupor, moderate to severe hemiparesis

5 Deep coma, decerebrate posturing, moribund appearance

Table 2. World Federation of Neurological Surgeons Scale (Open Table in a new window)
Grade Glasgow Coma Scale Score Clinical Findings
I 15 No headache or focal signs
II 15 Headache, nuchal rigidity, no focal signs
III 13-14 Headache, nuchal rigidity, no focal signs
IV 7-12 Headache, rigidity, focal signs
V 3-6 Headache, rigidity, focal signs

Table 3. Fisher Grade (Open Table in a new window)
Grade CT Findings
1 No blood detected
2 Diffuse thin layer of subarachnoid blood
3 Localized thrombus or thick layer of subarachnoid blood
4 Intracerebral or intraventricular hemorrhage with diffuse or no subarachnoid blood


Treatment
Medical Care
Prehospital care should include assessment of vital signs and neurological status. Airway, breathing, and circulation should be
addressed with endotracheal intubation, if necessary, and establishment of intravenous access.
Medical therapy of cerebral aneurysms involves general supportive measures and prevention of complications for individuals
who are in the periprocedural period or are poor surgical candidates. Treatment decisions should be based on the clinical status
of the patient, vascular anatomy of the aneurysm, and surgical or endovascular considerations.
Medical management of aneurysmal SAH is orchestrated in the ICU, with cardiac monitoring and placement of an arterial line.
Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel
blockers, and prevention of seizures.
Following surgical or endovascular aneurysm treatment, blood pressure is maintained at higher levels to diminish complications
associated with vasospasm. Vasospasm usually occurs between days 3 and 21, presenting with headache, decreased level of
consciousness, and variable neurological deficits. Serial TCD may be employed to detect trends in cerebral blood flow during
this period.
Induced hypertension, hypervolemia, and hemodilution (ie, "triple-H therapy") aimed to maintain adequate cerebral perfusion
pressure in the setting of impaired cerebrovascular autoregulation. However, guidelines have moved toward maintenance of
euvolemia and induced hypertension based on recent literature.[9]
Intraarterial papaverine or endovascular balloon angioplasty may be used to treat vasospasm in select patients.
Infectious aneurysms are friable, with an increased propensity for hemorrhage. Anticoagulation is avoided in this setting. As
these lesions resolve with antibiotic therapy, surgical approaches usually are deferred. Regression or evolution of these
aneurysms is monitored with serial angiography.
Unruptured Intracranial Aneurysms
The management of unruptured intracranial aneurysms is highly controversial. The International Study of Unruptured
Intracranial Aneurysms (ISUIA) indicated a relatively low risk of rupture in small aneurysms without history of SAH. Aneurysms
less than 10 mm in size had an annual rupture rate of approximately 0.05%. For posterior communicating,
vertebrobasilar/posterior cerebral, or basilar tip aneurysms less than 10 mm, the risk of rupture over 7.5 years approximated
2%, with all other locations harboring a risk of almost 0%. Recent guidelines and an evidence-based systematic review of the
literature have formulated recommendations for the care of patients with unruptured intracranial aneurysms, principally based on
age, history, and aneurysm size.
The anatomical characterization and morphology of unruptured aneurysms are not readily standardized, however. Some
investigators have advocated endovascular or surgical treatment of all aneurysms less than 10 mm if age is less than 50 years,
in the absence of contraindications. The presence of cigarette smoking, family history of aneurysms, polycystic kidney disease,
or systemic lupus erythematosus may elevate the risk of rupture and should be considered. Asymptomatic aneurysms greater
than 10 mm should also be considered for treatment, accounting for age, coexisting medical conditions, and relative risks for
treatment.
Considerable surgical mortality and morbidity rates at 1 year (as high as 3.8% and 15.7%, respectively) have been
demonstrated in preventive treatment of unruptured aneurysms. The surgeon's experience may be a significant and highly
variable factor in operative morbidity rate and functional outcome. More recently, application of diffusion-weighted MRI has
demonstrated silent thromboembolic events associated with endovascular treatment of unruptured cerebral aneurysms. Quality-
of-life issues, including the psychological morbidity of living with an unruptured intracranial aneurysm, also must be addressed.
Therapeutic decision making must balance endovascular or surgical morbidity and mortality rates with the risk of hemorrhage
and other considerations on an individual basis. Future studies in the management of unruptured intracranial aneurysms may
systematically account for the evolving technology of advanced endovascular approaches, detailed aneurysm morphology, novel
neuroimaging correlates, ethnic and geographical variation, neurocognitive impairment following endovascular or surgical
treatment, and quality-of-life issues.

Surgical Therapy
Microsurgical techniques focus on excluding the aneurysm from the cerebral circulation and reducing mass effects on adjacent
structures. Various approaches have been developed and tailored to the anatomy and location of the aneurysm. A surgical clip
usually is placed across the aneurysm neck with preservation of the parent vessel, eliminating any aneurysmal rests that may
redevelop subsequently. Alternative techniques involve proximal or Hunterian ligation, wrapping the aneurysm, and trapping (ie,
combined proximal and distal vessel occlusion).
Adjunctive measures have been developed to reduce operative morbidity and to provide cerebral protection. Aneurysmal
rupture, the principal surgical complication, may be avoided with induced hypotension, CSF drainage, diuretics, hyperventilation,
and use of minimal brain retraction. Hypothermia, with or without circulatory arrest, and systemic hypotension are used
commonly. A large study of mild intraoperative hypothermia, however, failed to demonstrate benefit of this adjunctive technique.
Lumbar spinal drainage allows relaxation of brain parenchyma and provides a clean surgical field. Postoperative angiography is
performed routinely to check for major vessel occlusion or persistence of an aneurysmal rest. Operative morbidity rate increases
with aneurysm size (2.3% for < 5 mm; 6.8% for 6-15 mm, 14% for 16-25 mm) and varies by location.
Optimal timing of aneurysm surgery depends on the clinical status of the patient and associated factors. Early surgery (ie, < 48-
96 hours after SAH) is favored for candidates in good condition or those with unstable blood pressure, seizures, mass effect
from thrombus, large amounts of blood, or evidence of aneurysm growth or rebleeding. Early surgery carries an increased
operative morbidity, although the risks of vasospasm and rebleeding are reduced considerably.
Delayed surgery (ie, 10-14 d after SAH) may be considered for large aneurysms in difficult locations or for candidates in poor
clinical condition. Surgery is indicated for ruptured or symptomatic aneurysms in patients without extenuating contraindications
or considerably advanced age. Surgery generally is precluded if the clinical status is poor, corresponding to Hunt and Hess
grade 4 or 5.
Endovascular Techniques
Advances in endovascular techniques have provided therapeutic alternatives that may be employed even in the setting of acute
aneurysmal SAH. These techniques allow parent vessel preservation and may be combined with surgical approaches.
Electrolytically detachable platinum coils (eg, Guglielmi detachable coils [GDC]) may be deployed strategically within the
aneurysm, promoting thrombosis and eventual obliteration. Wide-neck aneurysms may be more difficult to occlude with these
devices. Other materials, such as balloons or glue, also may be used. Complications include vessel perforation, hemorrhage, or
distal thromboembolism.
Endovascular therapy or coiling of cerebral aneurysms has proliferated during the past of particular cerebral aneurysms are
likely influenced by numerous factors. The International Subarachnoid Aneurysm Trial (ISAT) demonstrated the superiority of
coiling with improved clinical outcomes. Seizures were also less common in patients with endovascular treatment, yet late
rebleeding was also more common. Selection bias may also have influenced ISAT and, therefore, treatment for a given
individual must still be tailored to each case.
A meta-analysis of relevant studies (including ISAT) found that endovascular coiling of cerebral aneurysms yields a better
clinical outcome than clipping does, with the benefit greatest in patients with a good preoperative grade.[1, 2] The analysis also
confirmed, however, that there is a greater risk of rebleeding with coiling, particularly for patients with a poor preoperative grade.
Patient mortality at 1 year with coiling was not significantly different from 1-year mortality with clipping.[1, 2]
Progressive refinement in endovascular techniques and devices tailored for the cerebrovasculature have expanded therapeutic
options available for definitive treatment of cerebral aneurysms. More pliable, low-profile stents may be used for stent-assisted
coiling for obliteration of wide-necked aneurysms.
Self-expanding or balloon-expandable covered stents may be used for treatment of selected carotid or vertebral artery
pseudoaneurysms.[10] The Silk flow-diverter stent allows complete occlusion in most cases after 1 year of treatment, with 7.8%
permanent morbidity and 3% mortality.[11]
Large or giant intracranial aneurysms may be treated with a combination of devices, such as stent-assisted coil placement.[12]
However, the requirement of dual antiplatelet therapy in stent-assisted coiling may increase the risk of intracranial hemorrhage.
[13]
Refinement of endovascular techniques for very small intracranial aneurysms has expanded treatment options, yet
complications may also increase in this particular subset.[14]

Although endovascular coiling is a feasible, effective treatment for many elderly patients with ruptured and unruptured
intracranial aneurysms, careful patient selection is crucial in view of the risks of the procedure, which may outweigh the risk of
rupture in some patients with unruptured aneurysms, according to a systematic review and meta-analysis that included 21
studies of 1511 patients aged 65 years or older.[15, 16]
In this study, long-term occlusion was achieved in 79% of patients.[16] The rate of perioperative stroke (4%) was similar for
patients with unruptured and ruptured aneurysms. Intraprocedural rupture occurred in 1% of patients with unruptured aneurysms
and in 4% of patients with ruptured aneurysms. Perioperative mortality was 23% for patients with ruptured aneurysms and 1%
for those with unruptured aneurysms. At 1-year follow-up, 93% of patients with unruptured aneurysms and 66% of patients with
ruptured aneurysms had good outcomes.
Consultations
A multidisciplinary approach to the treatment of cerebral aneurysms is recommended. The following specialists should be a part
of the multidisciplinary team:
Neurosurgeon
Interventional neuroradiologist
Neurologist
Rehabilitation specialist
Diet
Restrict possible surgical candidates to taking nothing by mouth (NPO).
Employ nasogastric feedings for individuals with a decreased level of consciousness.
Recommend a soft, high-fiber diet to alert patients; patients should avoid caffeine.
Activity
Advise bed rest in a quiet dark environment during the initial week following aneurysmal SAH.
Perform passive range of motion exercises and frequent turning.
Assist patients with self-care activities, followed by slow advancement in activity as tolerated.

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

Calcium channel blockers
Class Summary
These agents are administered to minimize sequelae of cerebral vasospasm.
Nimodipine (Nimotop)
For improvement of neurological impairments resulting from spasms following SAH caused by ruptured congenital intracranial
aneurysm in patients in good postictal neurological condition.
While studies show benefit in severity of neurological deficits caused by cerebral vasospasm following SAH, no evidence shows
that the drug either prevents or relieves spasm of cerebral arteries. Actual mechanism of action unknown but may involve
protection of brain against ischemia.
Therapy should start within 96 h of SAH. If capsule cannot be swallowed because patient undergoing surgery or unconscious, a
hole can be made at both ends of capsule with 18-gauge needle, and contents extracted into a syringe. Contents then can be
emptied into patient's nasogastric tube in situ and washed down tube with 30 mL isotonic saline.
Antiepileptics
Class Summary
These agents are administered for treatment and prevention of seizures.
Fosphenytoin (Cerebyx)
Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Following administration, plasma esterases
convert fosphenytoin to phosphate, formaldehyde, and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and
decreases seizure activity.
To avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium
doses, express dose as phenytoin sodium equivalents (PE). Although can be administered IV and IM, IV is route of choice and
should be used in emergency situations.
Concomitant administration of IV benzodiazepine usually necessary to control status epilepticus. Full antiepileptic effect of
phenytoin, whether given as fosphenytoin or parenteral phenytoin, not immediate.
Antihypertensives
Class Summary
These agents help in controlling systemic blood pressure.
Labetalol (Normodyne, Trandate)
Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, thereby decreasing blood pressure.
Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.
Analgesics
Class Summary
These agents help in pain relief.
Morphine sulfate (MSIR, Duramorph, Astramorph, MS Contin)
Drug of choice for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Various IV doses used; commonly titrated until desired effect obtained.
Antiemetics
Class Summary
These agents help in minimizing nausea and vomiting.
Prochlorperazine (Compazine)
May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and
depressing reticular activating system. In addition to antiemetic effects, has advantage of augmenting hypoxic ventilatory
response, acting as respiratory stimulant at high altitude.
Antacids
Class Summary
These agents help in relieving gastrointestinal acid reflux.
Ranitidine (Zantac)
Inhibits stimulation of H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and
hydrogen-ion concentration.
Stool softeners
Class Summary

These agents help in softening stools and minimizing straining.
Docusate sodium (Colace, Dialox, Surfak, Regulax, Sulfalax)
For patients who should avoid straining during defecation; allows incorporation of water and fat into stool, causing stool to
soften.

Follow-up
Further Outpatient Care
See the list below:
After hospital discharge, continue physical, occupational, and speech therapy.
Administer medications for vasospasm and to prevent complications such as seizures, urinary tract infections, or venous
thromboses.
Following definitive treatment of a cerebral aneurysm with either endovascular or surgical obliteration, serial imaging
studies should be obtained as an outpatient. Various imaging modalities, including CTA, 1.5 or 3T MRA, and conventional
angiography may be used. The use of noninvasive angiographic techniques for serial evaluation has grown in recent
years.[17]
Further Inpatient Care
Following neurosurgical or endovascular intervention, continued care in the ICU generally includes the following:
Serial neurologic examinations
Avoidance of hypotension or hypertension (mean arterial pressure [MAP] should be in the range of 70-130 mm Hg)
Use of isotonic solutions, such as normal saline, to minimize cerebral edema
Treatment or prophylaxis of seizures
Treatment of urinary tract infections
Prevention of venous thrombosis
Prophylaxis for gastric ulcers
Physical, occupational, and speech therapy
Repeat CT scan in case of clinical deterioration
Inpatient & Outpatient Medications
See the list below:
Nimodipine for vasospasm
Phenytoin for prevention or treatment of seizures
Transfer

Immediately after prehospital evaluation and emergent stabilization, transfer patients with aneurysmal SAH to a center with
neurosurgical expertise.
Deterrence/Prevention
See the list below:
Prevention of neurological injury necessitates definitive treatment of a diagnosed cerebral aneurysm.
Patient education regarding symptoms of aneurysmal rupture may be important, as 10% of individuals die before
reaching medical attention.
Noninvasive screening with CTA or MRA is important in patients with medical conditions associated with cerebral
aneurysms or a family history of SAH or aneurysms.
Recent data showing superior functional outcomes and reduced complications for those on statins prior to aneurysmal
SAH may promote the use of statins.
Complications
See the list below:
Vasospasm
Recurrent hemorrhage
Seizures
Hydrocephalus
Hyponatremia
Cardiac arrhythmia, myocardial infarction, or congestive heart failure
Neurogenic pulmonary edema, pneumonia, or atelectasis
Gastrointestinal bleeding
Anemia
Venous thromboembolism
Prognosis
See the list below:
Prognosis of aneurysmal SAH has been associated with the following:
Age
Neurological status on admission
Aneurysm location
Number of days after SAH of admission (ie, delay from SAH to hospital admission)
Presence of hypertension and other medical illnesses
Degree of vasospasm

Degree of SAH
Extent of intraparenchymal or intraventricular hemorrhage
Outcome assessments following aneurysmal SAH may not be properly evaluated with the use of a single scale or
measure. Cognitive dysfunction and subjective experience of recovery should also be considered.
Patient Education
See the list below:
Educate regarding the warning signs and symptoms of SAH.
Educate regarding potential risk factors for aneurysmal SAH, including the following:
Hypertension
Cigarette smoking
Illicit drug use
Alcohol
For excellent patient education resources, visit eMedicineHealth's Headache Center. Also, see eMedicineHealth's patient
education article, Brain Aneurysm.

Questions & Answers
Overview
What is the mortality rate for aneurysmal subarachnoid hemorrhage (SAH)?
What are symptoms of cerebral aneurysms?
What are physical findings indicative of cerebral aneurysms?
What are neurologic findings suggestive of cerebral aneurysms?
What are the characteristics of aneurysmal subarachnoid hemorrhage (SAH)?
What is the role of lab studies in the diagnosis and assessment of cerebral aneurysms?
What is the role of imaging studies in the diagnosis of cerebral aneurysms?
What is included in nonsurgical treatment of cerebral aneurysms?
What is the role of surgery in the treatment of cerebral aneurysms?
What is the role of endovascular coiling in the treatment of cerebral aneurysms?
What are cerebral aneurysms?
How are saccular aneurysms characterized?
What are aneurysmal subarachnoid hemorrhages (SAH)?
What is the pathogenesis of cerebral aneurysms?
Which conditions increase the risk for development of cerebral aneurysms?
What causes dolichoectatic aneurysms of proximal vessel?
What is the pathophysiology of infectious cerebral aneurysms?

What is the pathogenesis of traumatic cerebral aneurysms?
What causes neoplastic aneurysm formation?
Which conditions are caused by vein of Galen aneurysms?
What is the progression of aneurysmal rupture?
What is the prevalence of cerebral aneurysms in the US?
What is the global incidence of aneurysmal subarachnoid hemorrhage (SAH)?
What are the mortality rates for cerebral aneurysms?
What are the racial predilections of cerebral aneurysms?
How does the prevalence of cerebral aneurysms vary by sex?
How does the prevalence of cerebral aneurysms vary by age?
Presentation
Which clinical history is characteristic of cerebral aneurysms?
What are the symptoms of cerebral aneurysms and subarachnoid hemorrhage (SAH)?
Which physical findings are characteristic of cerebral aneurysms?
Which neurological findings suggest cerebral aneurysms?
What are anterior communicating artery (ACoA) aneurysms?
What are anterior cerebral artery aneurysms?
What are middle cerebral artery (MCA) aneurysms?
What are posterior communicating artery (PCoA) aneurysms?
What are internal carotid artery (ICA) aneurysms?
What are basilar artery aneurysms?
What are vertebral artery or posterior inferior cerebellar artery aneurysms?
What are false localizing signs of cerebral aneurysms?
What are causes of cerebral aneurysms?
DDX
What are the differential diagnoses for Cerebral Aneurysms?
Workup
What is the role of lab studies in the diagnosis of cerebral aneurysms?
What is the role of imaging studies in the workup of cerebral aneurysms?
What is the role of CT scanning in the workup of cerebral aneurysms?
What is the role of MRI in the workup of cerebral aneurysms?
What is the role of angiography in the workup of cerebral aneurysms?
Which imaging studies may be helpful in the workup of cerebral aneurysms?
Which cardiac tests may be helpful in the workup of cerebral aneurysms?
What is the role of lumbar puncture (LP) in the workup of cerebral aneurysms?

Which histologic findings are characteristic of cerebral aneurysms?
How are cerebral aneurysms staged?
Treatment
What is included in prehospital care for cerebral aneurysms?
What are the medical treatment options for cerebral aneurysms?
What conditions must be managed prior to definitive treatment for cerebral aneurysms?
What care is needed following surgical or endovascular cerebral aneurysm treatment?
What is the role of triple-H therapy in the treatment of cerebral aneurysms?
What is the role of intraarterial papaverine or endovascular balloon angioplasty in the treatment of cerebral aneurysms?
How are infectious cerebral aneurysms managed?
What are treatment guidelines for unruptured intracranial aneurysms?
What are the treatment options for unruptured intracranial aneurysms?
What is the role of surgery in the treatment of unruptured intracranial aneurysms?
What is the basis of treatment selection for unruptured intracranial aneurysms?
What are the surgical approaches to the treatment of cerebral aneurysms?
What measures are used to reduce operative morbidity in the treatment of cerebral aneurysms?
What is the role of lumbar spinal drainage the treatment of cerebral aneurysms?
What is the optimal timing of surgery for cerebral aneurysms?
When is surgical delay indicated for the treatment of cerebral aneurysms?
What is the role of endovascular techniques in the treatment of cerebral aneurysms?
What is the efficacy of endovascular therapy for cerebral aneurysms?
What are the advantages of low-profile stents in the treatment of cerebral aneurysms?
What are the indications for self-expanding covered stents in the treatment of cerebral aneurysms?
Which endovascular techniques are used for treatment of large or giant intracranial cerebral aneurysms?
What are considerations regarding endovascular coiling for the treatment of cerebral aneurysms in elderly patients?
Which specialists should be included on a multidisciplinary treatment team for cerebral aneurysms?
Which dietary modifications are used in the treatment of cerebral aneurysms?
Which activity restrictions are used in the treatment of cerebral aneurysms?
Medications
Which medications are used in the management of cerebral aneurysms?
Which medications in the drug class Stool softeners are used in the treatment of Cerebral Aneurysms?
Which medications in the drug class Antacids are used in the treatment of Cerebral Aneurysms?
Which medications in the drug class Antiemetics are used in the treatment of Cerebral Aneurysms?
Which medications in the drug class Analgesics are used in the treatment of Cerebral Aneurysms?
Which medications in the drug class Antihypertensives are used in the treatment of Cerebral Aneurysms?

Which medications in the drug class Antiepileptics are used in the treatment of Cerebral Aneurysms?
Which medications in the drug class Calcium channel blockers are used in the treatment of Cerebral Aneurysms?
Follow-up
What is included in outpatient care following treatment for cerebral aneurysms?
What is included in ICU care of cerebral aneurysms?
Which medications are used in the treatment of cerebral aneurysms?
What are the indications for transfer of patients with cerebral aneurysms?
How are is neurological injury prevented in cerebral aneurysms?
What are possible complications of cerebral aneurysms?
What is the prognosis of cerebral aneurysms?
What is included in patient education for cerebral aneurysms?

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

David S Liebeskind, MD, FAAN, FAHA, FANA is a member of the following medical societies: American Academy of Neurology,
American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of
Neuroradiology, National Stroke Association, Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy;
Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of
Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service,
Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical
Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological
Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American
Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

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

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke
Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory

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Additional Contributors
Draga Jichici, MD, FRCPC, FAHA Associate Clinical Professor, Division of Medicine, Department of Critical Care Medicine and
Neurology, Co-Director, Neurosurgical Intensive Care Unit, Co-Director, Transcranial Doppler Ultrasound, Hamilton Health
Sciences, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCPC, FAHA is a member of the following medical societies: American Academy of Neurology, Canadian
Critical Care Society, Canadian Medical Protective Association, Canadian Neurocritical Care Society, Canadian Neurological
Sciences Federation, Neurocritical Care Society, Royal College of Physicians and Surgeons of Canada


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