eMedicine Specialties > Radiology > Brain/Spine

Brain, Aneurysm

Federico C Vinas, MD, Consulting Neurosurgeon, Department of Neurological Surgery, Halifax Medical Center
Harvey I Wilner, MD, Clinical Associate Professor, Department of Radiology, Wayne State University

Updated: Dec 30, 2008

Introduction

Left oblique cerebral angiogram in a patient with multiple intracranial aneurysms shows an anterior communicating aneurysm and a middle cerebral artery aneurysm. The patient underwent a frontotemporoparietal craniotomy, during which surgical clips were placed in both lesions in one setting.

Left oblique cerebral angiogram in a patient with a proximal intracranial internal carotid artery aneurysm. The surgical approach to this aneurysm requires a craniotomy with an orbitotomy and drilling of the anterior clinoid process; however, this aneurysm has a favorable neck-to-fundus ratio for endovascular coil placement.

Image obtained after the placement of a Guglielmi detachable coil in the aneurysm. The patency of the internal carotid artery and all its branches is preserved. Contrast material does not fill the aneurysm.

Background

The word "aneurysm" comes from the Greek word aneurysma (ana, meaning across, and eurys, meaning broad) and denotes an abnormal dilatation of an artery. Cerebral aneurysms involve both the anterior circulation and the posterior, or vertebrobasilar, circulation. Anterior circulation aneurysms arise from the internal carotid artery or any of its branches, whereas posterior circulation aneurysms arise from the vertebral artery, basilar artery, or any of their branches.^1,2

Intracranial aneurysms are named according to the artery, the segment of origin, or both; for example, anterior communicating aneurysms arise from the anterior communicating artery, and posterior communicating artery aneurysms arise from the internal carotid artery near the origin of the posterior communicating artery. Intracranial aneurysms are classified into saccular and nonsaccular types on the basis their shape and etiology. Nonsaccular aneurysms include atherosclerotic, fusiform, traumatic, and mycotic types. Saccular, or berry, aneurysms have several anatomic characteristics that distinguish them from other types of intracranial aneurysms. Typically, saccular aneurysms arise at a bifurcation or along a curve of the parent vessel, or they point in the direction in which flow would proceed if the curve were not present.

For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education article Aneurysm, Brain.

Pathophysiology

Origin of intracranial aneurysms and risk factors

Several theories attempt to explain the origin of intracranial aneurysms. Initially, a defect in the internal elastic lamina of arterial walls was postulated as the mechanism responsible for the genesis of saccular, intracranial aneurysms; however, numerous histologic and experimental studies failed to reveal evidence that supports this theory. Currently, the most important pathogenetic factor in aneurysmal formation is considered to be mural degeneration in regions of hemodynamic stress.

Many risk factors are correlated with the development of intracranial aneurysms and related aneurysmal subarachnoid hemorrhage (SAH). These factors include arterial hypertension, cigarette smoking, female sex, use of analgesics, and a genetic predisposition. The incidence of intracranial aneurysms is increased in patients with connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, polycystic kidney disease, coarctation of the aorta, and intracranial arteriovenous malformations.

Aneurysmal size

With time, most intracranial aneurysms increase in size, rupture, or both. Juvela et al reported a series of 181 cases of unruptured aneurysms.³  The initial median diameter was 4 mm; the follow-up period was 13.9 years. In 17 of 27 patients who experienced hemorrhage, aneurysmal size clearly increased over time. Among patients with intracranial aneurysms that were 10 mm or larger in diameter, the estimated rupture rate 7 years after diagnosis was 24%.

On the basis of findings from autopsy series and cranial magnetic resonance angiography (MRA) examinations, the prevalence of small unruptured and asymptomatic aneurysms is significant. Ruptured aneurysms are usually larger than unruptured ones. Some investigators believe that once aneurysms reach a certain critical size, the probability of hemorrhage increases. Aneurysmal rupture depends on multiple factors, such as the patient's age, a history of smoking, and cocaine use. In the literature, aneurysms that are 5-10 mm are considered to be at risk for bleeding. This information is an estimated average of the findings from multiple series published between 1969 and 1999.

In a study of 181 unruptured aneurysms in 142 patients who were observed for at least 10 years, 67% of the aneurysms that ruptured were initially smaller than 6 mm.³ Among 1,092 patients who were included in the Cooperative Aneurysm Study between 1970 and 1977, the average maximum diameter of ruptured aneurysms was 8.2 mm. Thirteen percent of the ruptured aneurysms were smaller than 5 mm in diameter. Unruptured asymptomatic aneurysms were smaller than 10 mm in 94% of the cases. The size of unruptured symptomatic aneurysms varied: 70% were 3-10 mm in diameter, and 13% were larger than 25 mm. Only 2-3% of ruptured aneurysms were giant.

An earlier Cooperative Aneurysm Study was conducted between 1958 and 1965 and included 2,349 single ruptured aneurysms. Unfortunately, the data from this study may not be completely accurate because only 24% of the patients underwent bilateral carotid and vertebral angiography.

There are hundreds of reports of brain aneurysms. As a neurosurgeon, the author often admits patients with SAH and aneurysms of 5-7 mm to the hospital for care.

Aneurysmal multiplicity

The prevalence of aneurysmal multiplicity is generally higher in autopsy series (25-31%) than in large clinical series (15-24%). Female patients account for 60-81% of patients with multiple aneurysms. The internal carotid and middle cerebral arteries seem to be prone to the formation of multiple aneurysms. In the literature, the rate of multiple aneurysms varies widely, ranging from 4% to 35%. In a series of 400 patients with intracranial aneurysms who were admitted to a hospital in the United Kingdom, 108 had multiple intracranial aneurysms. Other authors report a 20% incidence of multiple aneurysms and a 5% association with arteriovenous malformations.

A review of the literature published between 1941 and 1979 revealed that 13% of cases of multiple aneurysms were diagnosed at angiography; the range was 4-33%. In a series of 380 patients, the incidence of multiple intracranial aneurysms was 8.7%. In Hino et al's series of 462 patients with ruptured aneurysms, 20% had bilateral aneurysms. In a series of 494 surgically treated aneurysms reported by Inci et al, the incidence of multiple aneurysms was 35%.⁴

The reported incidence of multiple intracranial aneurysms is extremely variable. Factors that affect the reported incidence include the patient population; whether the series included surgical, radiologic, or autopsy findings; and whether the aneurysms were ruptured or unruptured. On the basis of the author's experience and the data from the literature, a general rule is that 10% of aneurysms are multiple, 10% are bilateral, and 10% involve the posterior circulation.

Complications of SAH

Despite substantial improvement in the management of patients with aneurysmal subarachnoid hemorrhage, including early aneurysm occlusion by endovascular techniques and surgical procedures, a significant percentage of patients with SAH still experience serious sequelae, such as neurological or cognitive deficits, as a result of primary hemorrhage, secondary injury mechanisms, or both.^5,6,7,8,9,10

Complications after SAH may be divided into medical complications and neurologic ones. Although most major morbid conditions and deaths related to SAH are attributed to neurologic complications such as aneurysmal rebleeding and vasospasm, medical complications significantly contribute to morbidity in these patients and are responsible for 23% of the deaths.

Fluid and electrolyte abnormalities are relatively common in patients with SAH. Hyponatremia, which is present in 35% of patients with SAH, is probably the most common abnormality. In most patients, natriuresis results from abnormal secretion of the atrial natriuretic factor that produces urinary loss of sodium (ie, cerebral salt wasting). Clinically, hyponatremia may exacerbate alterations in the patient's level of consciousness and cause seizures and cerebral edema. Distinguishing the syndrome of inappropriate atrial natriuretic factor from the syndrome of inappropriate antidiuretic hormone secretion is important. In the former, patients are sodium depleted and hypovolemic, whereas in the latter, patients are normovolemic or hypervolemic. Fluid restriction in a patient with incipient hyponatremia and hypovolemia secondary to natriuresis may be detrimental, particularly in those with cerebral vasospasm.

Arrhythmias and waveform abnormalities on electrocardiograms (ECGs) are common immediately after the hemorrhage and are likely to be associated with both the initial loss of consciousness and the sudden death that can occur after SAH. Arrhythmias have been recorded in 91% of patients after the onset of SAH. Although these arrhythmias are usually benign, ventricular tachycardia and ventricular fibrillation can be life threatening. Serious arrhythmias are more likely to occur in patients with hypokalemia, in patients of advanced age, or in those who exhibit a prolonged QT interval; therefore, continuous ECG monitoring is recommended in all patients with SAH.

Regarding pulmonary complications, severe hypoxia may occur in the period immediately after SAH as a result of aspiration pneumonia or, less frequently, neurogenic pulmonary edema.

The most common neurologic complications in patients with SAH are rebleeding, vasospasm, and hydrocephalus. Aneurysmal rebleeding is the most serious and disabling event after SAH. The highest frequency of rebleeding—4%—occurs the first day after SAH; the incidence decreases to 1.5% per day over the following 13 days. Approximately 15-20% of patients experience rebleeding within 2 weeks, and 50% experience rebleeding within 6 months after SAH. Mortality rates associated with rebleeding are 70-90%. Early surgical or endovascular treatment of the aneurysm eliminates the potential for rebleeding. In the first 14 days after aneurysmal SAH, angiographic vasospasm occur in approximately 70-90% of patients. The incidence of vasospasm is correlated with the amount of blood in the subarachnoid space. Half of these patients have an ischemic stroke.

The frequency of acute hydrocephalus during the first 3 days after aneurysmal SAH is estimated to be approximately 20%; however, the reported incidence of acute hydrocephalus after SAH varies widely. Reported incidences in the literature range from 12% to 63%. In a series of 3,521 patients admitted to the hospital within 3 days of the hemorrhage, computed tomography (CT) scans obtained at admission showed hydrocephalus in 15% of cases. In another series, the incidence of acute hydrocephalus was 20%. Chronic hydrocephalus develops in 10-37% of patients who survive aneurysmal SAH. Radiologic findings that are correlated with the development of hydrocephalus include the presence of intraventricular blood and focal areas of thick layers of subarachnoid blood. A significant number of patients without intraventricular hemorrhage have chronic symptomatic communicating hydrocephalus.

Frequency

United States

In patients with connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, polycystic kidney disease, coarctation of the aorta, and intracranial arteriovenous malformations, the incidence of intracranial aneurysms is increased.

Saccular, or berry, aneurysms are more frequent in the anterior circulation (ie, the carotid circulation), whereas fusiform aneurysms are more common in the vertebrobasilar system. Overall, intracerebral aneurysms include approximately 85-95% of the aneurysms in the carotid system, with 30% of those being in the anterior communication artery – anterior cerebral artery complex, 25% being in the posterior communicating arteries, 20% being in the middle cerebral arteries, 10% being in the basilar artery, and approximately 5% being in the vertebral arteries.

International

The incidence of intracranial aneurysms is unknown because most aneurysms remain undetected until they rupture or produce neurologic deficits. Autopsy studies reveal that approximately 5% of adults have a cerebral aneurysm; however, more than 50% of aneurysms identified at postmortem examinations are asymptomatic and were previously unrecognized. More is known about the incidence of ruptured aneurysms. In Western countries, the average annual incidence of subarachnoid hemorrhage (SAH) is approximately 10 cases per 10,000 people.

A low incidence of intracranial arterial aneurysms has been reported in some regions, including India, Iran, and many parts of Africa.

Mortality/Morbidity

Ruptured intracranial aneurysms are associated with high morbidity and mortality rates. Approximately 10-20% of affected patients die before reaching the hospital; approximately 8% die from progressive deterioration related to the initial hemorrhage. In patients with SAH who go untreated, the risk of rebleeding is 4.1% on the first day and then 1.5% per day for the following 2 weeks. By 6 months, 50% of patients with SAH have repeated bleeding at least once. After 6 months, the risk of rebleeding stabilizes at approximately 3% per year. Without treatment, approximately 18% of patients with subarachnoid hemorrhage (SAH) are functional survivors at 10 years, 8% are disabled, and 74% will have died. After surgical or endovascular treatment, one third of patients with SAH achieve good functional and neurologic outcomes.

Race

There are differences in the incidence of cerebrovascular disease and intracranial aneurysm related to race and ethnicity.

• A low incidence of intracranial arterial aneurysms has been reported in some regions, including India, Iran, and many parts of Africa.

• An analysis of findings in 244 patients in Detroit revealed a white-to-black ratio of 2.3:1 for intracranial aneurysms; however, when only patients who had SAH and bleeding aneurysms were considered, the ratio was 1.6:1.

• In a study by Bruno et al, the incidence of aneurysmal SAH among Hispanic residents of New Mexico was approximately 2.5 times higher than that among non-Hispanic whites; this finding suggests that the prevalence of berry aneurysms is higher in Hispanics or that there is a greater tendency to rupture.¹¹

Sex

The patient's gender influences the prevalence of aneurysms in certain anatomic locations. In female patients, the most common aneurysmal location is the supraclinoid segment of the internal carotid artery. In male patients, the most common site of ruptured aneurysms is the anterior communicating complex, whereas the most common reported site of unruptured aneurysms is the supraclinoid carotid artery. Female patients are more likely than male patients to have aneurysms of the ophthalmic, cavernous, or posterior communicating segments of the internal carotid artery.

Age

Intracranial aneurysms are diagnosed more frequently in middle-aged patients than in other patients. Fox documented a peak incidence of symptomatic aneurysms in patients 30-40 years of age; by contrast, in 2 cooperative studies, the peak incidence occurred in those 40-50 years of age. Intracranial aneurysms are rare in children and are more likely to be associated with vascular anomalies, trauma, infection, or systemic disease. Symptomatic aneurysms in children have a peculiar predilection for the carotid bifurcation.

Anatomy

The internal carotid artery enters the petrous portion of the temporal bone at the base of the skull through the carotid canal. Within the petrous bone, the carotid artery courses vertically and then turns horizontally at its genu to travel in an anteromedial direction, forming the carotid siphon. As the carotid artery passes above the foramen lacerum and under the gasserian ganglion, it penetrates the lateral dural ring and turns medially, forming the lateral carotid loop, and enters the cavernous sinus. In the cavernous sinus (ie, the cavernous segment), the carotid artery proceeds in a superomedial direction toward the posterior clinoid process. At the level of the posterior clinoid, the carotid artery turns forward, forming the medial loop. The meningohypophyseal trunk originates at this level. The carotid then exits the cavernous sinus and enters the subarachnoid space.

The ophthalmic segment of the internal carotid artery extends from the distal dural ring to the origin of the posterior communicating artery. This is the longest subarachnoid segment of the internal carotid artery. It possesses 2 major bends that create areas of hemodynamic stress that predispose it to aneurysm formation. The first bend, best depicted on lateral angiographic views, occurs as the carotid artery ascends and bends sharply in a posterior direction after it penetrates the dura. The second bend, best appreciated on a dorsal or anteroposterior angiographic view, is a gentler medial-to-lateral curve that occurs as the artery courses medial to the anterior clinoid process and laterally arcs to ascend toward the bifurcation.

The ophthalmic segment has 2 major branches: the ophthalmic artery and the superior hypophyseal artery. The ophthalmic artery usually arises immediately beneath the optic nerve, and the superior hypophyseal artery arises from the medial or ventromedial surface of the carotid, below the anterior clinoid process. Ophthalmic aneurysms typically arise along the first bend of the internal carotid artery, distal to the origin of the ophthalmic artery, and project either dorsally or dorsomedially toward the optic nerve. Superior hypophyseal artery aneurysms usually arise from the inferomedial surface of the internal carotid artery and project superomedially. The posterior communicating artery originates from the posteromedial surface of the internal carotid artery and penetrates the membrane of Liliequist to join the posterior cerebral artery inside the interpeduncular cistern.

Several perforators originate from the carotid or posterior communicating artery — namely, the anterior thalamoperforating arteries. Posterior communicating aneurysms project posteriorly and slightly inferiorly.

The choroidal segment of the internal carotid artery begins at the origin of the anterior choroidal artery and ends at the carotid bifurcation. The anterior choroidal artery arises distal and lateral to the posterior communicating artery. The internal carotid artery then bifurcates into the anterior and middle cerebral arteries.

The middle cerebral artery begins at the bifurcation of the internal carotid artery and courses along the sylvian fissure. It may be divided into the following 4 segments: (1) an M1 segment, located between the carotid bifurcation and the genu, (2) an M2 segment, which courses over the insular surface, (3) an M3 segment, which traverses the opercular surface of the sylvian fissure to reach the cortical surface, and (4) a distal M4 segment, consisting of its cortical branches.

The vertebral artery enters the subarachnoid space at the cranio-occipital junction. The first branch is the posterior spinal artery, which descends into the spinal cord. The vertebral artery then courses medially and superiorly around the medulla. The most important branch is the posterior inferior cerebellar artery, which travels in a posterolateral direction, just inferior to the oliva.

The basilar artery begins at the vertebrobasilar junction and courses superiorly toward the interpeduncular fossa. The first major branch of the basilar artery is the anterior inferior cerebellar artery, which courses laterally and posteriorly to supply the inferior surface of the cerebellum. The superior cerebellar artery originates just proximal to the basilar bifurcation and courses laterally to supply the superior cerebellar hemisphere. The basilar artery terminates in the interpeduncular fossa, where it bifurcates into the posterior cerebral arteries.

The posterior cerebral artery consists of 3 segments: (1) the P1 segment, which extends from its origin at the basilar bifurcation to its junction with the posterior communicating artery and contains several posterior thalamoperforating arteries; (2) the P2 segment, which courses through the crural and ambient cisterns, serving as the origin of the anterior temporal, hippocampal, medial posterior choroidal, peduncular perforating, middle temporal, posterior temporal, and lateral posterior choroidal arteries; and (3) the P3 segment, which courses through the quadrigeminal cistern toward the calcarine fissure, where it divides into the calcarine and parieto-occipital arteries.

Presentation

In a review of the literature, 89% of saccular intracranial aneurysms were associated with subarachnoid hemorrhage (SAH), 7% were associated with a mass effect, and 4% were incidental findings. Warning signs, such as a sentinel leak or aneurysmal expansion, frequently precede aneurysmal rupture. The classic description of SAH that results from a ruptured intracranial aneurysm is a sudden and explosive headache that the patient describes as the worst headache of his or her life. Patients have different degrees of mental status change. A massive release of catecholamines accompanies SAH and, frequently, induces myocardial changes that may cause lethal arrhythmias, pulmonary edema, or heart failure.

Clinical findings in survivors of aneurysm rupture vary, depending on the origin, location, and severity of the hemorrhage. Bleeding confined to the subarachnoid space usually produces nonfocal symptoms and signs of increased intracranial pressure and meningeal irritation, including headache, confusion, photophobia, nausea, vomiting, blurred vision, nuchal rigidity, and cranial nerve palsies. Nuchal rigidity often occurs within 6-24 hours. On examination, the Kerning sign and the Brudzinski sign may be positive. A positive Kerning sign is pain in the hamstrings when the legs are straightened; a positive Brudzinski sign is involuntary hip flexion with neck flexion.

Focal neurologic deficits are often indicative of a related ischemic infarct or mass effect from an intracranial hematoma. The type of deficit depends on the location and size of the clot, which may cause cranial neuropathies, visual field cuts, or speech deficits. Although several clinical grading scales for SAH have been proposed, the Hunt and Hess classification is used most widely. The Hunt and Hess clinical classification of SAH is as follows:  

• Grade 1 — Headache, slight nuchal rigidity
• Grade 2 — Cranial nerve palsy, severe headache, nuchal rigidity
• Grade 3 — Mild focal deficit, lethargy, confusion
• Grade 4 — Stupor, moderate to severe hemiparesis, early decerebrate rigidity
• Grade 5 — Deep coma, decerebrate rigidity, moribund appearance

This clinical grading system is correlated with treatment and patient outcome. A higher Hunt and Hess grade is generally thought to be correlated with a higher incidence of vasospasm and a poorer outcome. Although the literature contains some statistics, establishing accurate percentages in relationship to the Hunt and Hess grade or the Fisher grade is difficult. Intensive medical treatment of patients with aneurysmal SAH has improved perioperative treatment and significantly improved the subsequent outcome.

Traditionally, the outlook for patients with an SAH of grade IV or V has been dismal, whereas in many series of patients with an aneurysm of Hunt and Hess grade I, II, or III, good neurologic recovery has occurred in 60-90% of patients. In addition to the Hunt and Hess grade at presentation, size and location of the aneurysm and patient age also affect surgical morbidity.

Regarding aneurysmal size, a study revealed morbidity rates of 2.3% for aneurysms smaller than 5 mm, 6.8% for aneurysms 5-15 mm, and 14% for aneurysms 16-25 mm. Morbidity rates also vary with aneurysmal location, with a 4.8% morbidity rate for posterior communicating aneurysms, 8.1% for middle cerebral artery aneurysms, 11.8% for ophthalmic aneurysms, 15.5% for anterior communicating aneurysms, and 16.8% for carotid bifurcation aneurysms. The morbidity rate is reported to be 6.5% for patients younger than 45 years, 14% for those 45-64 years of age, and 32% for patients older than 64 years.

Preferred Examination

A strong clinical suspicion of aneurysm may be validated by the use of several diagnostic studies, including CT, lumbar puncture, magnetic resonance imaging (MRI), and cerebral angiography. CT is typically the first diagnostic test ordered when there is a possibility of SAH. Findings on a nonenhanced CT scan may confirm subarachnoid blood in more than 90% of patients with acute SAH. Diffuse, severe subarachnoid hemorrhage (SAH) is seldom helpful in identifying the specific site of the aneurysm. Localized SAH, however, may be highly indicative of the site of aneurysm rupture, as in cases in which blood is present in the sylvian fissure as a result of a rupture of a middle cerebral artery (MCA) trifurcation aneurysm or in cases in which interhemispheric blood is present between the anterior part of the frontal lobes as a result of the rupture of an aneurysm of the anterior communicating artery.

In the author's opinion, the use of high-resolution CT angiography combined with the use of digital substraction angiography with dynamic rotational views provides the best possible visualization of the flow pattern and characteristics of any intracranial aneurysm.

Limitations of Techniques

In patients with diffuse SAH, CT scans may not depict the site of aneurysm rupture. In severely anemic patients with a small hemorrhage, false-negative CT findings do occur, although rarely. Small amounts of SAH may be cleared from the cerebrospinal fluid (CSF) and may not be visible as areas of increased attenuation on CT scans as soon as 1 or 2 days after the initial severe headache; therefore, a nonenhanced CT scan of the head obtained after this time may show false-negative findings of SAH.

Differential Diagnoses

Brain, Arteriovenous Malformation

Other Problems to Be Considered

Thunderclap headache
Benign orgasmic cephalgia

Computed Tomography

Nonenhanced CT scan of a middle-aged man with headaches. The patient had a giant aneurysm of the left internal carotid artery in its intracavernous segment. This aneurysm is densely calcified and is easily depicted.

Findings

CT is usually the initial diagnostic procedure when SAH is suspected (see Image above and Image 6 in Multimedia). A good-quality nonenhanced CT scan may depict subarachnoid hemorrhage (SAH) in more than 90% of patients who undergo scanning within 48 hours, depending on the location and extent of the subarachnoid blood and the time elapsed since ictus. The location of the subarachnoid blood identifies the presumed location of the ruptured aneurysm, a finding often supported by the demonstration of an aneurysm in the area of maximum clot localization or the area of the maximum amount of subarachnoid blood.^{12,13,14,15,16,17}

In particular, CT is useful in patients with multiple aneurysms. In addition to indicating the location of the vascular lesion, a CT scan may show unsuspected anomalies, such as a related arteriovenous malformation, intraparenchymal hematoma, or hydrocephalus. Finally, by providing a quantitative measure of the amount of blood in the subarachnoid cisterns and ventricles, the initial CT scan provides a reliable predictive index that may be used to identify patients who are likely to have a vasospasm. Most often, the Fisher grading system is used to classify SAH; this system is based on the amount of blood visible on the CT scan. The Fisher grading system is as follows:

• Grade 1 — No subarachnoid blood detected
• Grade 2 — Diffuse vertical layers thicker than 1 mm
• Grade 3 — Localized clot and/or vertical layer thicker than 1 mm
• Grade 4 — Intracerebral or intraventricular clot with diffuse or no subarachnoid blood

The advent of high-resolution CT angiography with the implementation of dynamic 3D reconstructions allows for a superb visualization of the intracranial vessels, as well as the anatomy and characteristics of the aneurysm; images with a similar resolution enable the visualization of intracranial vessels. However, it does not show progression on the pattern of flow. Although some authors have suggested that high-resolution CT angiography may replace cerebral angiography, in the author's opinion, high-resolution CT angiography complements digital substraction angiography but should not replace it.

Degree of Confidence

Subarachnoid bleeding is demonstrated in more than 90% of patients, depending on the location and extent of the subarachnoid blood and the time elapsed since ictus.

False Positives/Negatives

Lumbar puncture is usually reserved for the screening of patients with potential sentinel bleeding or for confirming the presence of bleeding in patients whose clinical history is suggestive but whose CT findings are negative.

Magnetic Resonance Imaging

T1-weighted magnetic resonance image (MRI) of a middle-aged woman with progressive headaches, aphasia, and right-sided hemiparesis. A large intracerebral mass with a significant amount of surrounding edema is depicted. The lesion is a giant internal carotid artery aneurysm.

T2-weighted MRI of a middle-aged woman with progressive headaches, aphasia, and right-sided hemiparesis. The lesion is a giant internal carotid artery aneurysm. Note the flow void, the blood breakdown products within the layers of mural thrombus, and calcification within the aneurysm that produces a marked hypointense signal. Significant surrounding edema is depicted.

Findings

MRI can provide additional details about the regional anatomy and the size, shape, and content of an aneurysm (see Images above and Images 1-2 in Multimedia). Most intracranial aneurysms appear as an area of flow void larger than the healthy vessels in that region. Their interior usually enhances significantly after the intravenous administration of gadolinium–diethylenetriamine penta-acetic acid. Most giant aneurysms have calcifications and an intraluminal clot, but their residual lumen may be depicted as a region of flow void. The thrombosed areas may have variable signal intensity, which represents blood products at different stages. MRIs may also depict small amounts of parenchymal blood surrounding the aneurysms; this finding indicates which of the multiple aneurysms have bled.^{18,19,20,21,22,23}

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. 

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

MRA is useful in detecting intracranial aneurysms in both symptomatic patients and asymptomatic patients. MRA is a noninvasive and sensitive method of testing for an aneurysm in symptomatic patients who are at high risk (ie, patients with polycystic renal disease and those with 1 or more first-order family members with documented cerebral aneurysms).

In the symptomatic patient, MRA often reveals the site of aneurysmal dilation. Two main types of MRA—the time-of-flight technique and the in-flow technique—are used more often than the phase-sensitive or the phase-contrast technique. For both time-of-flight and in-flow sequences, a large set of axial source images are acquired; these are then reformatted into images that appear similar to conventional angiograms. The most common method used is the maximum intensity projection (MIP) method.

Advances in MRI technology, including the use of newer 3T units, enable excellent visualization of the intracranial vessels. The use of high-resolution magnetic resonance angiography is appropriate for the follow-up of patients who have undergone treatment with endovascular coiling; it accurately delineates residual aneurysm necks and parent vessel patency (in the absence of a stent) and enables excellent visualization of contrast filling within the coil mass. However, when a stent has been placed in the parent artery, MRI may not be appropriate, owing to the presence of artifacts.²³

Degree of Confidence

MRI alone is sensitive in the evaluation of subarachnoid and intraparenchymal hemorrhage. Small aneurysms may be missed. MRA is more sensitive to small aneurysms, and it can reliably depict lesions as small as 3-4 mm; however, for optimal sensitivity, MIP images should always be viewed in conjunction with the source images; small aneurysms may be missed if only the MIP images are reviewed. At the present time, angiography should still be considered the criterion standard for the detection of small aneurysms.

Ultrasonography

Findings

In patients with subarachnoid hemorrhage (SAH), transcranial Doppler (TCD) ultrasonography is a noninvasive technique that is useful in detecting vasospasm of the intracranial arteries. Most measurements are obtained by using particular cranial windows of relatively thin bone. The most common cranial window is the transtemporal one, which is located above the zygoma. This window is used to measure velocities of the middle cerebral artery, the anterior cerebral artery, the distal internal carotid artery, and the proximal posterior cerebral artery. The transorbital window enables measurement of the ophthalmic artery and the internal carotid artery; the suboccipital window enables measurement of the vertebral arteries and the basilar artery.

In addition, TCD ultrasonography provides repeated serial measurements that may show a pattern of increasing velocities, which lead to clinical deterioration. Clinical decision-making, such as decisions concerning the initiation and duration of hypervolemic, hypertensive therapy, may be aided by TCD.

Nuclear Imaging

Findings

Some giant aneurysms in the cavernous segment of the internal carotid artery may be treated with occlusion of the artery. Treatment of these lesions depends heavily on the demonstration of cerebrovascular reserve, which is the ability to tolerate temporary or permanent carotid artery occlusion. This reserve is assessed by means of an endovascular balloon occlusion test, with qualitative or quantitative cerebral blood flow measurements at single-photon emission CT (SPECT) scanning. Patients who can tolerate balloon occlusion and have no significant areas of hypoperfusion on SPECT scans are candidates for carotid occlusion.

Angiography

Left oblique cerebral angiogram in a patient with multiple intracranial aneurysms shows an anterior communicating aneurysm and a middle cerebral artery aneurysm. The patient underwent a frontotemporoparietal craniotomy, during which surgical clips were placed in both lesions in one setting.

Left oblique cerebral angiogram in a patient with a proximal intracranial internal carotid artery aneurysm. The surgical approach to this aneurysm requires a craniotomy with an orbitotomy and drilling of the anterior clinoid process; however, this aneurysm has a favorable neck-to-fundus ratio for endovascular coil placement.

Image obtained after the placement of a Guglielmi detachable coil in the aneurysm. The patency of the internal carotid artery and all its branches is preserved. Contrast material does not fill the aneurysm.

Findings

Cerebral angiography remains the definitive preoperative diagnostic tool in patients with intracranial aneurysms (see Images above and Images 3-5 in Multimedia). Angiography may also be used to detect and evaluate aneurysmal multiplicity or other associated vascular diseases, assess collateral circulation, identify congenital anomalies, and diagnose cerebral vasospasm and aid in their treatment.

A routine angiographic examination consists of a selective 4-vessel study, including both internal carotid and both vertebral arteries. This study enables the evaluation of the cerebral circulation to determine the source of subarachnoid hemorrhage (SAH) and to identify other concomitant lesions that may influence the surgical plan.

Multiple views are often necessary to delineate the origin of vessels overlapping the aneurysms and the configuration of the aneurysm neck. In the anterior circulation, carotid ophthalmic aneurysms are often best seen on the lateral or 45° oblique projection. Posterior communicating and anterior choroidal aneurysms are usually well profiled on the lateral and oblique projections.

Carotid bifurcation aneurysms and some middle cerebral aneurysms may warrant the use of a straight anteroposterior, or Caldwell, projection. The basal, or submental vertex (SMV), projection may help define the anatomy of middle cerebral aneurysms. In the posterior circulation, oblique projections are useful in showing the basilar bifurcation, posterior inferior cerebellar aneurysms, or aneurysms of the vertebrobasilar junction. Occasionally, a straight anteroposterior view may be required to depict an aneurysm of the posterior inferior cerebellar artery.

Intervention

Endovascular balloon test occlusion with qualitative or quantitative cerebral blood flow and/or carotid artery pressure measurements have been successfully used to assess the hemodynamic risk of permanent or temporary carotid arterial occlusion. This assessment couples the 20-minute clinical occlusion test with a qualitative or quantitative test. Patients who cannot tolerate a balloon occlusion test of the internal carotid may require an extracranial-to-intracranial bypass and subsequent reevaluation before indirect treatment is initiated. The type of bypass is directly related to the flow deficiency.

Patients with frankly failing results during the clinical balloon occlusion test are at the greatest risk and pose the greatest challenge. Patients with an aneurysm in the cavernous sinus in whom the balloon occlusion test fails should be treated during extracranial-intracranial bypass surgery with a superficial temporal artery graft or a saphenous vein graft. The rate of blood flow supplied by a superficial temporal artery is 20-60 mL/min; this may not be enough to accommodate a normal blood flow of 75-120 mL/min through a middle cerebral artery. No collateral blood supply flows through the posterior and anterior communicating arteries. Higher flow rates may be achieved with a saphenous vein graft bypass.

During the past decade, the endovascular treatment of intracranial aneurysms has developed extensively. The original indication—the treatment of giant unclippable intracranial aneurysms— has been extended to include small aneurysms and those that have recently ruptured. The introduction of coils, stents, and newer materials allows for successful treatment of many intracranial aneurysms. Depending on the location, configuration, and characteristics of the aneurysm, consideration should be given to a surgical obliteration or endovascular treatment of an intracranial aneurysm.

It is the author's opinion that a team approach involving the neurosurgeon and the endovascular neuroradiologist is of paramount importance for the successful treatent of these patients. In many patients with intracranial aneurysm, a complex endovascular approach that takes into consideration the use of detachable coils, stents, balloons, and aneurysm neck remodeling increases the probability of a successful aneurysm occlusion. The use of hydrogel-coated coils for the endovascular treatment of intracranial aneurysms offers the theoretical advantages of increased volumetric occlusion, thrombus stabilization, and improved neointimal healing.^6,7,8,10,18

After the initial diagnosis of an intracerebral aneurysm, when symptoms or TCD ultrasonographic findings suggest vasospasm, repeat angiography definitively depicts the presence, severity, and location of the vasospasm and the status of the aneurysm. Therapy for the regions of narrowing may then be performed with either balloon angioplasty or an infusion of vasodilators, such as papaverine.

Following subarachnoid aneurysmal hemorrhage, endovascular treatment of vasospasm should be implemented in patients who develop clinical or radiologic symptoms of brain ischemia, in conjunction with increased Doppler velocities, despite maximal medical treatment.^5,24 Treatment may be either pharmacologic or mechanical. Calcium and phosphodiesterase inhibitors may be administered. In Europe, intravasular nimodipine is widely used; in North America, nicardipine and verapamil are the major agents used, because intravenous nimodipine has not been approved by the FDA.

Papaverine was the drug of choice in the past; however, papaverine is now considered less desirable owing to its short duration of vasodilatation and the risk of aggravation of increased intracranial pressure. Balloon angioplasty has a long-lasting effect but may be applied only in cases involving spasm of proximal vessels. Complications of its use are rare but may be life threatening. The author recommends the use of a combined approach, including the intra-arterial administration of pharmacologic agents and the use of balloon angioplasty. I also recommend that the approach be maintained and that repeat angioplasty procedures be performed as often as the patient's condition warrants it.^{5,6,7,25,26,27,28,29,30,31,32}

Medicolegal Pitfalls

• With endovascular procedures, complications often occur during puncture. Subintimal threading of the catheter or needle may cause dissection syndromes and subsequent ischemic complications. Neck hematomas may develop, requiring termination of the procedure. Occasionally, a thrombus develops in the punctured artery, requiring surgery on an emergency basis. Neurologic deficits may occur during primary vessel puncture.
• During cerebral angiography, complications include arterial dissection and delayed arterial occlusion; arterial rupture; hemorrhagic infarction; and displacement of the surgical clips from the aneurysmal necks.
• During balloon angioplasty, ischemic complications may occur as a result of excessive occlusion times. Stenosis may also occur because the diameter of the noninflated balloon is equivalent to the vessel's diameter. In this situation, the balloon adds to ischemia of the vasospasm before dilation. Occasionally, the procedure is performed in a patient whose blood flow has been critically reduced before dilation. Only short periods of vasodilation are tolerated. The most feared complication of angioplasty is separation of the balloon from the catheter and its distal migration into the intracranial arterial tree; this most often occurs when a detachable balloon is used to occlude the aneurysm. To prevent ischemic complications, the smallest possible balloon and catheter and be selected, and they should be attached firmly. Dilations should be performed rapidly. Hemorrhagic complications occur because of rupture of the primary vessel or aneurysm.
• Aneurysmal rupture during cerebral angiography may occur as a result of traction, the performance of maneuvers near the aneurysmal neck, or catheter misplacement in the neck of an aneurysm that increases dynamic pressures in the aneurysm. One should always be prepared to perform open craniotomy promptly if the aneurysm ruptures. If a thrombus obstructs the vessel, a fibrinolytic such as urokinase or tissue plasminogen should be used immediately.
• A major source of complications of direct surgical treatment of aneurysms is ischemia. Because of the critical nature of the neural structures supplied by the perforating branches, especially during the surgical treatment of posterior circulation aneurysms, occlusion of the perforating vessels typically causes dramatic symptoms. Maneuvers that ensure the identification and liberation of all perforating branches from the aneurysm sac before clip placement are of paramount importance. Inspection after clip positioning is also crucial to ensure that any proximal vessels continue to fill. Major arterial branch occlusions, although less common, have dramatic consequences as well. These problems most often occur as a result of poor clip placement.
• The morbidity and mortality rates of intraoperative rupture during the surgical treatment of intracranial aneurysms can be significant. The operating surgeon must have access to vascular control; in addition, the surgeon should have a practiced set of steps to avoid this complication and should treat it as quickly and efficiently as possible. Techniques to reduce the incidence of intraoperative aneurysm rupture include the use of sharp dissection and complete dissection of the lesion before any attempt at clip placement. Should intraoperative rupture occur, tamponade is usually the quickest and most effective method of initial management. If tamponade fails to significantly reduce the hemorrhage, temporary arterial occlusion should be considered.
• Cranial nerve deficits are well-recognized deficits that occur after the treatment of intracranial aneurysms. The most common cranial nerve deficit in the treatment for basilar bifurcation or posterior communicating artery aneurysms is a temporary third cranial nerve palsy that results in ptosis and ophthalmoplegia. The likely cause is surgical manipulation. Deficits are usually short lived, and most patients recover within 3 months. Other causes include injury from poor clip placement.
• The frequency of acute hydrocephalus during the first 3 days after aneurysmal SAH is approximately 20%. The proportion of patients who have acute hydrocephalus concurrent with intraventricular hemorrhage is 35-65%. Treatment options for patients with SAH and acute hydrocephalus include observation and ventricular drainage. In patients who are asymptomatic in the early postbleeding period, observation in the presence of ventricular dilatation appears justified; approximately 1 in 3 patients have neurologic deterioration in the following few days.
• Among other injuries, the obstruction of venous drainage is a consequence of excessive retraction or injury to the bridging veins. Obstruction may result in the development of hemorrhagic infarction.

Multimedia

Media file 1: T1-weighted magnetic resonance image (MRI) of a middle-aged woman with progressive headaches, aphasia, and right-sided hemiparesis. A large intracerebral mass with a significant amount of surrounding edema is depicted. The lesion is a giant internal carotid artery aneurysm.

Media file 2: T2-weighted MRI of a middle-aged woman with progressive headaches, aphasia, and right-sided hemiparesis. The lesion is a giant internal carotid artery aneurysm. Note the flow void, the blood breakdown products within the layers of mural thrombus, and calcification within the aneurysm that produces a marked hypointense signal. Significant surrounding edema is depicted.

Media file 3: Left oblique cerebral angiogram in a patient with multiple intracranial aneurysms shows an anterior communicating aneurysm and a middle cerebral artery aneurysm. The patient underwent a frontotemporoparietal craniotomy, during which surgical clips were placed in both lesions in one setting.

Media file 4: Left oblique cerebral angiogram in a patient with a proximal intracranial internal carotid artery aneurysm. The surgical approach to this aneurysm requires a craniotomy with an orbitotomy and drilling of the anterior clinoid process; however, this aneurysm has a favorable neck-to-fundus ratio for endovascular coil placement.

Media file 5: Image obtained after the placement of a Guglielmi detachable coil in the aneurysm. The patency of the internal carotid artery and all its branches is preserved. Contrast material does not fill the aneurysm.

Media file 6: Nonenhanced CT scan of a middle-aged man with headaches. The patient had a giant aneurysm of the left internal carotid artery in its intracavernous segment. This aneurysm is densely calcified and is easily depicted.

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Keywords

brain aneurysm, cerebral aneurysm, abnormal arterial dilatation, intracranial aneurysm, berry aneurysm, endovascular procedures, radiological diagnoses, Guglielmi detachable coil, GDC

Contributor Information and Disclosures

Author

Federico C Vinas, MD, Consulting Neurosurgeon, Department of Neurological Surgery, Halifax Medical Center
Federico C Vinas, MD is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, American Medical Association, Congress of Neurological Surgeons, Florida Medical Association, and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Harvey I Wilner, MD, Clinical Associate Professor, Department of Radiology, Wayne State University
Harvey I Wilner, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Roentgen Ray Society, American Society of Neuroimaging, American Society of Neuroradiology, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey L Creasy, MD, Associate Professor, Associate Section Head, Division of Neuroradiology, Director, Neuroradiology Fellowship, Department of Radiology, Vanderbilt University
Jeffrey L Creasy, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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