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.
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Cerebral Aneurysms (Neurology)
Cerebral Aneurysm (Neurosurgery)
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
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Further Reading
Keywords
brain aneurysm, cerebral aneurysm, abnormal arterial dilatation, intracranial aneurysm, berry aneurysm, endovascular procedures, radiological diagnoses, Guglielmi detachable coil, GDC
