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You are in: eMedicine Specialties > Radiology > BRAIN/SPINE
Brain, Arteriovenous Malformation
Article Last Updated: Apr 3, 2007
AUTHOR AND EDITOR INFORMATION
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Author: Robert A Koenigsberg, DO, MSc, FAOCR, Director of Neuroradiology, Professor, Department of Radiology, Drexel University College of Medicine
Robert A Koenigsberg is a member of the following medical societies: American Osteopathic Association, American Society of Interventional & Therapeutic Neuroradiology, American Society of Neuroradiology, and Radiological Society of North America
Coauthor(s): Tina Maiorano, BS, Medical College of Pennsylvania-Hahnemann University; Jeffrey R Wasserman, DO, Staff Physician, Department of Diagnostic Radiology, Medical College of Pennsylvania-Hahnemann University Hospital
Editors: Lucien M Levy, MD, PhD, Director of Neuroradiology, Professor of Radiology, Department of Radiology, George Washington University Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; 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
Author and Editor Disclosure
Synonyms and related keywords: AVM, brain AVM, arteriovenous aneurysm, arteriovenous angioma, cerebrovascular malformations, pial AVMs, parenchymal AVMs, dural AVMs, vein-of-Galen aneurysm
INTRODUCTION
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* Introduction
* Differentials
* Radiograph
* CT SCAN
* MRI
* Ultrasound
* Nuclear Medicine
* Angiography
* Intervention
* Multimedia
* References
Background
An arteriovenous malformation (AVM) is a tangled cluster of vessels, typically located supratentorially, in which arteries connect directly to veins with no intervening capillary bed. The lesion may be compact, containing a core of tightly packed venous loops, or it may be diffuse, with anomalous vessels dispersed among normal brain parenchyma. A 1988 study of more than 500 patients showed that the core, or nidus, of a compact AVM was from 2-6 cm in diameter in 77%.
AVMs account for approximately 11% of cerebrovascular malformations; the more common venous angiomas account for 64%. AVMs are more likely than other types of vascular malformations to be clinically symptomatic. AVMs typically involve the brain but occasionally are associated with the spinal cord and its dura.
For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education article, Aneurysm, Brain.
Categorization of AVMs
AVMs are categorized by their blood supply. Pial or parenchymal AVMs are supplied by the internal carotid or vertebral circulation; dural AVMs, by the external carotid circulation; and mixed AVMs, by both. Most common are pial AVMs, which are almost exclusively congenital. Dural AVMs are relatively uncommon and theorized to be secondary to trauma, surgery, thrombosis of an adjacent venous sinus, or veno-occlusive disease. Mixed AVMs usually occur when the lesion is large enough to recruit blood vessels from both the internal and external carotid arteries. A pediatric variant of AVM is the vein-of-Galen aneurysm, in which an AVM drains to and dilates the great vein of Galen.
Pial AVMs tend to be asymptomatic until the second, third, or fourth decade of life. They most commonly manifest as spontaneous hemorrhage or seizure. Other clinical signs include headache and transient or progressive neurologic deficit. Dural AVMs typically feature pulsatile tinnitus, cranial bruit, headache, or hemifacial spasm. Infants with a vein-of-Galen malformation may present with hydrocephalus or severe congestive heart failure.
Saccular aneurysms occur in association with AVMs in 6-20% of patients. The preferred site for an AVM-associated aneurysm is a feeding artery. Venous and intranidal aneurysms occur less frequently. When aneurysms and AVMs occur together, they can cause intracranial or subarachnoid hemorrhage, though intracranial hemorrhage is more likely to stem from an AVM.
Imaging of AVMs
Overall, AVMs are imaged best by using MRI, which can uniquely show these lesions as a tangle of vascular channels that appear as flow voids. Nonenhanced CT is superior for visualizing the small foci of calcification often associated with AVMs, and it also may delineate hyperattenuating serpiginous vessels constituting the nidus.
Nonenhanced CT is valuable for demonstrating the extent of acute hemorrhage and hydrocephalus. Contrast-enhanced CT shows enhancement of the typical vascular channels. Magnetic resonance angiography (MRA) or CT angiography (CTA) may be adequate for initial or follow-up evaluation of an AVM. Demonstration of the aneurysms sometimes found on AVM feeding arteries may be accomplished by means of MRA, CTA, or catheter angiography.
Spetzler and Martin grading system
The Spetzler and Martin grading system attempts to predict risk of surgical morbidity and mortality by assigning points to an AVM on the basis of its size, the eloquence of the adjacent brain, and the pattern of venous drainage. The grading system includes 5 possible points. If the AVM is small ( <3 cm), 1 point is assigned, if medium (3-6 cm), 2 points; or if large (>6 cm), 3 points.
An eloquent brain region is one in which injury results in a disabling neurologic deficit, with 0 points for noneloquent and 1 point assigned for involvement of eloquent brain.
Lastly, an additional point can be earned when the AVM drains into the deep venous system.
The grade of a lesion is determined by summing the points in each of the 3 categories. Therefore, surgical treatment of a grade I AVM presents little risk of morbidity and mortality. By contrast, a grade V lesion is associated with significant risk. A grade VI AVM is described as an inoperable AVM that is associated with a totally disabling deficit or death.
Factors influencing treatment
Relevant factors in the decision to treat an AVM include patient and family preferences, Spetzler-Martin grade, lesion site and angioarchitecture, clinical presentation, neurologic status, patient age and past medical history, and pregnancy. Current treatment modes include direct microsurgical intervention, intravascular intervention (eg, embolization or balloon insertion), and radiosurgery. Large AVMs may require a combination of these modes over several sessions.
Pathophysiology
The pathogenesis of AVMs is not well understood. Because the malformations characteristically lack the capillary bed that normally intervenes between artery and vein, investigation into the pathogenesis of AVMs has focused on, among other things, the molecular differences between arteries and veins, capillary-bed morphogenesis, and inherited disorders of vasculogenesis.
A major recent discovery demonstrates that the endothelial cell population is not homogeneous, as was believed previously. On the contrary, arterial and venous endothelial cells express different receptors from the onset of angiogenesis. Ephrin-B2 is found on arterial cells but not venous endothelial cells, whereas ephrin-B4 is found on venous cells but not arterial endothelial cells. Angiogenesis is impaired in ephrin-B2 knockout mice. That the endothelial cells lining arteries and veins are molecularly distinct suggests a mechanism for defective vasculogenesis and angiogenesis.
In addition, the role of angiopoietins and their tyrosine kinase receptors is being explored. Angiopoietin 1 (ang-1) and its ligand, tie-2, may be crucial for vascular remodeling in the embryo. Ang-1 apparently controls the recruitment of pericytes and smooth muscle cell precursors to the blood vessel wall. Upregulation of tie-2 has been demonstrated in AVM vasculature. The improper recruitment of periendothelial cells can contribute to the dysvasculogenesis of the capillary bed.
The gene coding for endoglin (CD105), which is a transforming growth factor b–binding endothelial cell receptor, has been implicated in the pathogenesis of hereditary hemorrhagic telangiectasia (HHT) type 1. HHT, also termed Osler-Rendu-Weber disease, is an autosomal dominant disorder that causes AVMs in the brain, skin, and viscera. Analogously, its variant, HHT type 2, is caused by mutations in the gene coding for activin receptorlike kinase (ALK-1).
Mutations in Flt-1, a tyrosine kinase receptor for vascular endothelial growth factor (VEGF), result in thin-walled vessels of abnormally large diameter. Because the proper morphogenesis of the capillary bed probably depends on signaling between arteries and veins, any distortion of vessel anatomy or function may be expected to impair the process. Immunohistochemistry has demonstrated increased expression of VEGF in the vasculature of AVMs and the surrounding brain parenchyma.
Frequency
United States
The incidence in the United States is the same as that seen worldwide.
International
The incidence of AVMs is estimated to be 0.04-0.52%. A 1988 study of 5754 consecutive autopsies showed a total of 276 vascular malformations, 0.5% of which were AVMs.
Mortality/Morbidity
The cumulative lifetime risk that an intracranial AVM will eventually bleed is estimated to be 50%. Hemorrhage is more likely to be intracerebral (parenchymal) or intraventricular rather than purely subarachnoid.
* The risk of spontaneous intracranial hemorrhage is 2-3% per year. Each episode has a 10-15% rate of mortality and a 20-30% rate of permanent neurologic deficit.
*
* In the year after the first hemorrhage, the risk of rebleeding is 6%; thereafter, it decreases to 2-4%. Overall, hemorrhage is implicated in 29% of patient deaths.
*
* The risks associated with a residual AVM of any size are widely believed to be equivalent to the risks associated with untreated lesions; however, this statement is controversial.
Race
No clear correlation exists between race and the prevalence of AVMs. However, the 1:7 ratio of intracranial vascular malformations to intracranial saccular aneurysms in the overall population has been shown to increase to 1:4 in people of Asian descent.
Sex
* Most studies have shown a slightly increased preponderance of pial AVMs in men.
*
* Dural AVMs of the anterior cranial fossa occur more frequently in men than in women. Other dural AVMs occur more commonly in women.
Age
* Pial AVMs are present from birth, but they usually are asymptomatic until the second, third, or fourth decade, when hemorrhage, seizure, or other symptoms occur. More than 95% of patients develop symptoms before age 70 years.
*
* Dural AVMs, which most commonly involve the transverse, sigmoid, and cavernous sinuses, are believed to be acquired and to develop during adulthood. Patients with dural AVMs of the anterior cranial fossa may be congenital and may present with hemorrhage from a ruptured venous aneurysm.
Anatomy
Anatomic location
AVMs can be found throughout the CNS. They may be microscopic or large enough to involve an entire hemisphere of the brain. Grossly, angiographically invisible AVMs are termed cryptic vascular malformations, a name which suggests that the lesions are thrombosed completely. Most AVMs are small (2-4 cm, 42%) to moderately sized (4-6 cm, 35%).
Of AVMs, 90% are supratentorial and tend to occur at watershed areas (straddling > 1 vascular territory) and 10% are infratentorial. Of supratentorial AVMs, 70% are purely pial with no meningeal or dural vascular supply. The remainder of lesions are purely dural or a pial-dural mix. Approximately one half of posterior fossa AVMs are purely dural or a pial-dural mix.
Pial AVMs lie within brain parenchyma and derive blood from the cerebral arteries, namely the anterior cerebral artery (ACA), middle cerebral artery (MCA), or posterior cerebral artery (PCA). The rapid shunting of blood typical of pial AVMs is visualized as an abnormal tangle of blood vessels with early, and frequently rapid, venous drainage, uniquely demonstrated by catheter angiography. Most AVMs involving the ACA or its branches are purely pial.
Dural AVMs are almost always infratentorial. They most frequently drain into the transverse and sigmoid sinuses in the posterior fossa, but they may also involve the cavernous sinus, inferior petrosal sinus, superior sagittal sinus, or other areas of the brain or spinal venous system. The occipital artery and meningeal branches of the external carotid artery are the vessels that most commonly supply dural AVM components. Tentorial and small dural branches of the internal carotid artery and vertebral arteries may also contribute. Dural AVMs may be classified according to the sinus involved. Further, dural AVMs may be associated with venous outlet stenosis or obstruction.
Morphologic features
Morphologically, AVMs may be either compact or diffuse. Compact AVMs are characterized by a nidus formed by tightly packed entangled venous loops that are interconnected by small venules. Small amounts of nonfunctional brain tissue are found between the loops. When located supratentorially, compact AVMs are often wedge shaped and extend through both gray matter and white matter. Typically, the base of the wedge is parallel to the meninges, with the vertex pointing toward the ventricles or deep brain.
The venous loops of a compact AVM attach to shunting arterioles, communicating venules, and draining veins. The microscopic shunting arterioles are the terminal branches of angiographically visible feeding arteries. A feeding artery is by definition an artery that transfers arterial blood to the AVM core. That the feeding arteries send branches both to the AVM and to normal brain tissue significantly confounds treatment.
Feeding arteries and vessels
Feeding arteries are of 3 types. The circumferential feeding artery extends around the nidus and sends branches both to small arterioles connected to the nidus and to normal brain capillaries. Penetrating feeding arteries bisect the AVM core and send branches to it. Final feeding arteries either connect directly to an AVM loop or branch to shunting arterioles.
After arterial blood has circulated through the AVM nidus, it is drained by collecting veins, which then feed into larger veins and may be either superficial or deep. The larger veins ultimately join to connect to a major draining vein. Major draining veins course through the sulcus and are connected to the neighboring cortical veins by numerous venules. The distal end of a major draining vein is connected to large hemispheric veins, which drain into the venous sinuses.
AVMs are currently believed to be hemodynamically compartmentalized; each compartment has its own feeding arteries and draining veins. For example, a large AVM in the sensorimotor area may have a lateral compartment supplied by MCA branches, a medial compartment supplied by ACA branches, and a posterior compartment supplied by PCA branches. The number of compartments in an AVM is proportional to its size. An AVM smaller than 3 cm in diameter is likely to have 1 compartment, a 3-cm or 4-cm AVM may have 2 compartments, and an AVM larger than 4 cm in diameter typically has at least 3 compartments.
In contrast to the vessels of compact AVMs, those of diffuse AVMs are dispersed among normal brain tissue. Diffuse AVMs are typically found in the basal ganglia or thalamus. Blood flow through an AVM is proportional to the number of compartments and to AVM volume. For example, the rate of flow may be 285 mL/min for a 2-cm lesion and 800-1000 mL/min for a 4- to 5-cm lesion.
The vessels themselves are enlarged and dilated as a result of passive congestion secondary to increased pressure in the arterial core. Bright red blood under relatively high pressure often is seen in the veins of an AVM, owing to arteriovenous (AV) shunting. Occasionally, aneurysms develop in AVM vessels, which is consistent with the altered hemodynamic stress characteristic of the lesions. Therefore, aneurysms may develop along feeding arterial pedicles or along venous drainage pathways. Typically, the latter occurs proximal to a venous stenosis.
Histologic features
Histologically, distinguishing between the arteries and the arterialized veins of an AVM can be difficult because the wall thickness of each can vary unpredictably. Both feeding arteries and draining veins may be attenuated in some places and thickened by intimal hypertrophy in others. Greatly attenuated arterial or venous walls may be the source of hemorrhage. Within the vessel, atherosclerosis and thrombosis are common, presumably because of the unusually high volume of blood flow and the tortuosity and angulation of the vessels.
Regional blood flow in the area immediately surrounding an AVM may be reduced to approximately 81% of normal. This is referred to as the steal phenomenon. Accordingly, the neighboring gyri and underlying parenchyma often are discolored, infarcted, and atrophic as a result of chronic ischemia. Other typical features include gliosis, russet-colored pigmentation resulting from the presence of hemosiderin-laden macrophages after prior hemorrhage, and scattered foci of calcification. Overlying meninges may be thickened and fibrotic. Because AVMs are congenital lesions that replace normal brain tissue rather than displace it, they typically are not associated with mass effect unless hemorrhage has occurred. However, some AVMs do demonstrate mass effect, edema, and ischemic changes.
Despite the hypoperfusion seen in the normal brain parenchyma surrounding the AVM, total cerebral blood flow may be increased by as much as 50-100%. AVMs tend to exhibit slow progressive growth over many years because the shunted blood continually seeks adjacent vessels. Normal vasculature may be involved in the process.
Clinical Details
Symptoms
Symptoms of an AVM may include headache, weakness, numbness, visual problems, or most often, the abrupt onset of stroke. Usually, AVMs are clinically silent initially and then become symptomatic in the second, third, or fourth decade of life. Spontaneous rupture with hemorrhage is the presenting symptom in 30-55% of pial AVMs.
The annual risk for bleeding from an unruptured AVM is 2-4%. The annual risk for a ruptured lesion is 6% in the first year after hemorrhage and 2-4% thereafter. Overall, a history of hemorrhage is the best clinical predictor of future bleeding. Pial AVMs are more likely to bleed than are dural AVMs.
Angiographic findings
Angiography reveals certain features that are believed to correlate with an increased risk of hemorrhage. The features include the presence of associated intranidal, remote, or pedicular aneurysms; central or deep venous drainage; stenosis of a draining vein; and periventricular or intraventricular location. Natural-history studies have shown that a small nidus is another positive risk factor for hemorrhage, though whether this risk is overestimated because small unruptured AVMs are asymptomatic and because they often go undiagnosed is unclear.
Factors known to reduce the risk of hemorrhage include peripheral or mixed venous drainage and angiomatous change. Angiomatous change is the development of an anomalous transcortical supply to the AVM in response to chronic ischemia of the brain parenchyma adjacent to the lesion.
High flow within the AV shunt is believed to induce significant hypotension in the lesion's feeding arteries. This has been postulated to cause ischemic symptoms, such as seizure or prolonged or transient focal neurologic deficit, in some patients. Further study is needed to clarify the matter. Seizures also may result from gliosis of the margins surrounding the lesion, ischemia, or mass effect. Occasionally, seizures do not correspond to the site of the malformation.
An unruptured AVM may cause headaches, mimicking migraine or cluster headache. Headaches usually are ipsilateral to the lesion and are believed to stem from hydrocephalus, stretching of the dura, or increased pressure in the dural sinuses. In 16% of patients, headache may be the only presenting symptom.
Other problems to be considered
Clinically, a fundamental distinction is the differentiation of an AVM from a saccular aneurysm. A patient with an AVM is likely to present with a history of seizures and/or unilateral headache and a history of subarachnoid hemorrhage, particularly if it is mild. Because vascular malformations are under low pressure, blood tends to well rather than spurt out of the lesion during a rupture. Bleeding is often parenchymal or mixed over a hemisphere, away from the circle of Willis. In contrast, rupture of a saccular aneurysm usually involves massive arterial bleeding from the base of the brain, accompanied by arterial spasm. Consequently, patients bleeding from an aneurysm may be more seriously ill than those bleeding from an AVM.
A headache indistinguishable from migraine may occur ipsilateral to an unruptured AVM. The coexistence of migraine and seizures is particularly suggestive of a vascular malformation. Dural AVMs of the sigmoid or cavernous sinus also may produce migrainelike episodic headaches or pulsatile tinnitus.
Large AVMs are diagnosed easily with conventional angiography. However, smaller lesions may mimic malignant vascular brain tumors with AV shunting. AVMs may be distinguished by the more uniform caliber of their vessels; the characteristic dilatation of proximal arterial trunks; and the potentially huge, tortuous, and redundant draining veins. Although early venous filling/drainage typically results from vascular AVM, other causes include neoplasm (eg, glioblastoma multiforme, cerebral infarction, and an inflammatory mass).
On CT, an AVM that appears as a noncalcified mass or a calcified and hyperattenuating focal mass must be distinguished from other calcified masses, such as tuberous sclerosis, colloid cyst, neoplasm, and aneurysm.
When CT reveals parenchymal hematoma, possible causes (in addition to vascular malformation) include trauma; coagulopathy; hypertension; other vascular pathologies, such as aneurysm, amyloid angiopathy, or vasculitis; vascular occlusion, as from venous infarct or embolic stroke with reperfusion hemorrhage; infection; and neoplasm.
If abnormal intracranial calcifications are seen, the differential diagnosis includes congenital or developmental diseases; infection; endocrine or metabolic causes, such as hypercalcemia, hypoparathyroidism, lead encephalopathy, and carbon monoxide intoxication; other vascular causes, including aneurysm and atherosclerosis; hematoma resulting from trauma; neoplasm; and iatrogenic causes, such as radiation therapy and chemotherapy.
Dark areas on T2-weighted MRIs can be due to rapid blood flow, as from an AVM, aneurysm, or neoplasm; dense calcification, as from an AVM, infection, or neoplasm; or a variety of other causes not associated with vascular malformations. These include the presence of air, minerals or metals, hemorrhage, and mucinous or dense proteinaceous material.
Ring-enhancing lesions may result from a thrombosed vascular malformation or aneurysm, high-grade astrocytoma, primary lymphoma, metastasis, subacute infarct, resolving hematoma, abscess or fungal granuloma, demyelination, and radiation necrosis.
Preferred Examination
The first imaging study in patients with a suspected AVM is usually a CT or MRI. These studies are good for depicting an AVM, and they are relatively noninvasive, requiring an injection of contrast material into only a small vein.
Computed tomography
Brain CT is the imaging test for evaluating acute headache or other acute mental-status changes suggestive of acute cerebral hemorrhage. Detection of a lobar hemorrhage can suggest an underlying mass or AVM. Cerebral CT can be used to identify areas of acute hemorrhage, and the results can suggest a vascular malformation, particularly with the judicious use of contrast material. Further, CT can uniquely demonstrate vascular calcifications associated with AVMs.
Magnetic resonance imaging
Without use of radiation or invasive techniques, MRI can help identify and characterize AVMs of the CNS, including the brain and spinal cord. MRI is the examination of choice in patients with chronic headaches, seizure disorders of unknown etiology, and pulsatile tinnitus, among others.
MRI typically follows CT imaging in the acute setting of neurologic illness, when an underlying vascular lesion such as an AVM is suggested. MRI can demonstrate areas of parenchymal AVM involvement, showing both dilated feeding arteries and enlarged draining veins.
MRA and venography can further supplement conventional MRI in demonstrating in a near angiographic fashion the anatomy and microarchitecture of an AVM. MRI is the study of choice in the detection of vascular malformations of the spinal cord and spinal dura.
Angiography
Catheter angiography remains the criterion standard for characterization and delineation of brain and spinal AVMs. Angiography is a dynamic real-time study not only demonstrates the presence or absence of an AVM but also shows vascular transit time. Diagnostic angiography is uniquely able to delineate the size and number of feeding arteries and define the pial, dural, or mixed origin of the AVM.
Angiography can be used to measure the size of the AVM and judge the compactness of the nidus. Further, angiography can be used to evaluate the venous drainage pattern (superficial, deep, or mixed). In addition, angiography frequently depicts associated risk factors for hemorrhage, including aneurysms and venous stenosis. Planning angiography remains vital in both interventional neuroradiologic and neurosurgical evaluation of patients with AVM.
Limitations of Techniques
Computed tomography
CT is an excellent technique for detecting cerebral hemorrhage, but it can miss an underlying AVM. AVMs typically are isoattenuating relative to normal parenchyma and therefore can be overlooked, particularly if contrast agent is not administered. In an emergency setting, the administration of an iodinated contrast agent is typically deferred in favor of patient stabilization. Contrast CT also poses an inherent risk of radiation, and its cost tends to favor MRI as a better screening examination for AVM in the general population. However, contrast-enhanced CT is performed to detect cerebral AVM when MRI is contraindicated or otherwise not feasible.
Magnetic resonance imaging
MRI is excellent for demonstrating the AVM nidus and abnormal flow voids typical of an AVM. However, in acute cerebral hemorrhage, compressed AVMs may no longer demonstrate flow and therefore can be overlooked. This may lead to the need for serial MRI studies to search for an underlying cause of cerebral hemorrhage not shown on a single MRI study. MRI can cause underestimation of the number of feeding arteries and associated aneurysms, which might also be missed. Furthermore, MRI can be relatively poorly sensitive in detecting dural malformations. Gadolinium-based contrast material may be needed to demonstrate abnormal vascular channels.
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently 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. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. 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
movingor 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.
Angiography
Diagnostic angiography is the criterion standard for the evaluation of AVMs; however, it is invasive and carries risks related to catheter placement and contrast agents and their injection. Specific neurangiographic risks include stroke, arterial dissection, reactions to the contrast material, and renal insufficiency and/or failure, among others. Nevertheless, modern cerebral angiography remains a safe and reliable method for AVM analysis, with an overall complication rate of less than 1%. Spinal angiography can be tedious and is associated with the risk of spinal cord infarction.
DIFFERENTIALS
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* Authors and Editors
* Introduction
* Differentials
* Radiograph
* CT SCAN
* MRI
* Ultrasound
* Nuclear Medicine
* Angiography
* Intervention
* Multimedia
* References
Brain, Aneurysm
Brain, Capillary Telangiectasia
Brain, Cavernous Angiomas
Brain, Hypertensive Hemorrhage
Brain, MRI Appearance of Hemorrhage
Brain, Stroke
Other Problems to Be Considered
Saccular aneurysm
Headache indistinguishable from migraine, migraine and seizures, pulsatile tinnitus
Malignant vascular brain tumors with AV shunting
Glioblastoma multiforme, cerebral infarction, inflammatory mass
Calcified masses such as tuberous sclerosis, colloid cyst, neoplasm, and aneurysm
With parenchymal hematoma – Trauma, coagulopathy, hypertension, other vascular pathology, vascular occlusion, infection, neoplasm
With intracranial calcification - Congenital or developmental disease, infection, endocrine or metabolic cause, other vascular cause, hematoma from trauma, neoplasm, iatrogenic causes
Dark areas on T2-weighted MRI -- Rapid blood flow, dense calcification, other causes
Ring-enhancing lesion - Thrombosed vascular malformation or aneurysm, high-grade astrocytoma, primary lymphoma, metastasis, subacute infarct, resolving hematoma, abscess or fungal granuloma, demyelination, radiation necrosis
RADIOGRAPH
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* Authors and Editors
* Introduction
* Differentials
* Radiograph
* CT SCAN
* MRI
* Ultrasound
* Nuclear Medicine
* Angiography
* Intervention
* Multimedia
* References
Findings
Plain radiography is not a modern modality used for imaging cerebral AVMs. Nevertheless, abnormally dilated vascular channels can be seen on plain skull images. Further abnormal intracranial calcifications associated with AVMs can also be detected; these are suggestive of an AVM. These findings should prompt cross-sectional imaging.
Degree of Confidence
Degree of confidence is poor, since impressions on the calvarium can be seen normally.
False Positives/Negatives
Plain films of the skull are not considered diagnostic in the detection of AVMs of the CNS.
CT SCAN
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* Authors and Editors
* Introduction
* Differentials
* Radiograph
* CT SCAN
* MRI
* Ultrasound
* Nuclear Medicine
* Angiography
* Intervention
* Multimedia
* References
Findings
CT imaging of a brain AVM can show an isoattenuating-to-hyperattenuating hemispheric mass, and CT scans can detect an accompanying abnormal vascular supply. In the absence of hemorrhage, nonenhanced CT can demonstrate small foci of calcification in as many as 30% of patients (see Image 1). Other possible findings include cystic cavities representing previous hemorrhage and hypoattenuating of surrounding parenchyma representing encephalomalacia, cerebral atrophy, or gliosis.
Contrast CT can demonstrate serpiginous vascular enhancement uniquely typical of an AVM. Occasionally, CT can demonstrate edema, mass effect, or ischemic changes that can be associated with an AVM, and further contrast imaging may identify small AVMs missed by plain CT examination.
In the hyperacute stage of hemorrhage, pial AVM appears as a hyperattenuating parenchymal lesion on nonenhanced CT because CT attenuation values and blood hemoglobin concentrations are directly proportional. Attenuation increases in the acute stage as a result of clot formation and the resulting increase in hemoglobin concentration. The hyperattenuating region may be surrounded by a rim of hypoattenuation caused by extruded serum and edema.
Because the attenuation of a hematoma decreases with time, the ruptured hemorrhagic component of an AVM evolves through a stage of isoattenuation to normal brain parenchyma. Therefore, nonenhanced lesions viewed during the isoattenuating phase may appear almost normal or may shine through, appearing minimally abnormal. If intravenous contrast material is administered during this stage, vascular enhancement may be seen, as well as nonspecific or ringlike areas of enhancement.
An AVM in the chronic stage of intracerebral hemorrhage appears hypoattenuating relative to normal brain tissue. In general, AVM enhancement that is not contiguous with the site of hemorrhage points to an associated aneurysm or venous varix.
Dural AVMs can be visualized by CT imaging.
In an emergency setting, CT imaging can show a presenting cerebral or extra-axial hemorrhage. CT imaging may show secondary signs, inferring the presence of a dural AVM, ie, abnormal enlarged dural sinuses or draining cerebral veins. Typically, these are appreciated best using contrast imaging. Unfortunately, the dural malformation nidus is typically demonstrated poorly on CT images alone.
Degree of Confidence
With CT, the degree of confidence is moderate. Typically, an additional study, such as MRI or catheter angiography, is necessary to confirm the presence of an AVM, but this is not always needed.
False Positives/Negatives
False-positive CT results may occur with lesions demonstrating enhancement or calcifications. Tumor neovascularity occasionally mimics an AVM, particularly that of a neovascular glioblastoma multiforme. In addition, a wide variety of CNS abnormalities can be associated with CNS calcifications, leading to false-positive results.
False-negative results may occur if an AVM is isoattenuating relative to regional parenchyma. Some lesions may be detectable only if iodinated contrast is administered. Further, an AVM may be overlooked if it is compressed by an adjacent parenchymal hemorrhage. Lastly, vascular AVMs can be misconstrued as cerebral hemorrhage because of large hyperattenuating vessels. Contrast CT or supplemental MRI or MRA can help clarify difficult cases.
MRI
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* Authors and Editors
* Introduction
* Differentials
* Radiograph
* CT SCAN
* MRI
* Ultrasound
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Findings
MRI findings
On MRI, the typical unruptured AVM appears as a tightly packed or loose tangle of vessels (see Image 2).
Rapid blood flow through enlarged arteries causes a signal or flow void on routine spin-echo T1- and T2-weighted images. This finding is uniquely characteristic of an AVM.
MRI can show lesion size and usually the primary supply of the AVM and its venous drainage. MRI can further demonstrate associated aneurysms on arterial feeders and associated sequelae such as mass effect, edema, or ischemic changes.
Vascular steal in the brain or spinal cord adjacent to the lesion may be visualized as a region of abnormal reduced signal intensity on T1-weighted images and increased signal intensity on T2-weighted, proton density—weighted; and short-tau inversion recovery images.
MRI is particularly well suited to document AVM rupture. The appearance of the lesion depends on the stage of the hematoma.
An acute hemorrhage is isointense on T1-weighted images and hypointense on T2-weighted images because of the presence of deoxyhemoglobin in extravasated but unlysed erythrocytes. A subacute intraparenchymal hemorrhage is hyperintense on both T1- and T2-weighted imaging, consistent with the presence of methemoglobin. Chronic hematoma is characterized by a central hyperintense core surrounded by a ring of hypointensity due to the presence of hemosiderin deposits in macrophages in the surrounding brain. Hemosiderin is mildly hypointense on T1-weighted images and markedly hypointense on T2-weighted images.
MRI is an excellent preoperative planning tool for delineating the relationship between an AVM nidus and critical brain structures. In particular, the relationship between hemispheric AVMs and eloquent brain regions can be clarified, particularly with functional MRI. Associated aneurysms may be seen within a hematoma as a flow void. Unfortunately, the sensitivity of MRI to aneurysms smaller than 1-2 cm is low.
Postoperative MRI
Postoperative MRI is useful for studying the effect of surgery on the adjacent brain; however, documentation of complete obliteration of the nidus is performed best with conventional angiography because MRI may fail to depict small amounts of residual nidus or persistent AV shunting. MRI can show the extent of nidal, arterial, or venous thrombosis following embolization. T2-weighted imaging is particularly useful for the detection of embolic complications.
Magnetic resonance angiography
MRA is a noninvasive alternative to conventional angiography. Certain lesions hidden on conventional angiograms may be identified only on MRIs because of their ability to depict hemosiderin deposits or other evidence of blood breakdown. Blood-breakdown products appear in a time-dependent manner after intracranial hemorrhage.
MRA offers several advantages over conventional angiography. For example, because of its ability to image all vessels in a given volume nonselectively, an AVM with multiple feeding arteries can be imaged noninvasively in a single study. In addition, 2-dimensional (2D) and 3-dimensional (3D) phase-contrast MRA can be used to examine the direction, rate, and quantity of blood flow. Another advantage of MRA is the ability to retrospectively examine images in any plane.
3D time-of-flight (TOF) angiography may be used to image the fast-flow components of AVMs. With flip angles of approximately 15º and a repetition time (TR) of 40 ms usually is adequate for saturating the stationary background tissues while allowing the visualization of fully magnetized inflowing blood. Slower-flowing components of the AVM tend to be visualized poorly without the use of an MRI contrast agent because the vessels become more saturated as they course through the imaging volume. This is not entirely undesirable, as it allows an unobstructed view of the feeding arteries and nidus by effectively suppressing overlying venous structures.
The arterial supply may be identified by means of 3D TOF, phase-contrast slab, or 3D phase-contrast acquisitions. Visualization of vessels with angiomatous change may require phase-contrast slab angiograms encoded for low flow velocities, eg, velocity encoding (Venc) = 20 cm/s. Otherwise, imaging with Venc of 80-100 cm/s typically demonstrates the arterial supply. Complex flow in the AVM nidus is seen best on 3D TOF acquisitions, using small voxel size, partial echo sampling, and a short echo time (TE).
Degree of Confidence
With MRI, the degree of confidence is high. MRIs of vascular malformations of the brain are unique and typically diagnostic of cerebral or spinal AVMs with a high degree of confidence. MRI findings may prompt catheter angiography for confirmation and preoperative or postoperative AVM treatment.
False Positives/Negatives
False-positive results may occur when other types of CNS vascular malformations are encountered; examples include cavernous angiomas, venous angiomas, and capillary telangiectasias. Lesions are associated with a lower risk of rupture but can mimic the appearance of an AVM, yet they lack characteristic AV shunting. Nevertheless, false-positive findings may prompt catheter angiography for clarification. MRI can further show abnormally enlarged arteries (atriomegaly), which are suggestive of an underlying malformation when none is present.
False-negative MRI findings of CNS AVMs occasionally can occur as a result of a small AVM or an inconspicuous location. AVMs may be overlooked or not apparent if they are compressed by an adjacent hematoma. AVMs can also be missed if they are indistinguishable from the flow void of an adjacent normal vessel.
ULTRASOUND
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* MRI
* Ultrasound
* Nuclear Medicine
* Angiography
* Intervention
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Findings
Typically, ultrasound is not used in evaluating cerebral AVMs. Ultrasonography may play an adjunctive role during open neurosurgery for the purposes of AVM localization.
NUCLEAR MEDICINE
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* Intervention
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Findings
Isotopic cerebral blood flow studies largely have been supplanted by modern CT, MRI, and digital subtraction angiography of the brain in the evaluation of AVMs.
Single-photon emission CT and positron emission tomography of the brain are useful for imaging ischemic penumbra surrounding a vascular lesion. Further, they may be helpful in the functional imaging of normal parenchyma surrounding a vascular malformation. This discussion is currently beyond the scope of this article.
ANGIOGRAPHY
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Findings
Conventional cerebral angiography is the criterion standard for the evaluation of AVMs (see Images 6-10). The study should include both internal carotid arteries and both vertebral arteries, with sequential evaluation of the arterial, capillary, and venous phases. External carotid arteries should be evaluated for dural contributions. The goal of the study should be to identify the number and location of feeding arteries, the angiographic location and size of the nidus, the shunt type of the lesion (eg, high flow vs low flow), and the pattern of venous drainage (eg, superficial, deep, or mixed).
On conventional angiography, patent pial AVMs have enlarged cerebral or spinal arteries and veins, rapid AV shunting, and early draining veins.
Dural malformations typically have slower flow or AV shunting and are supplied by dural vessels such as the meningeal branches or occipital arteries of the external carotid arteries or meningeal branches of the internal carotid or vertebral arteries.
Catheter angiography usually can be used to map all malformation feeders (pial, dural, or mixed), and it can be used to accurately access the size of the nidus.
Spetzler and Martin proposed a commonly used classification scheme to predict the surgical outcome. This scheme is typically applied to angiographic data described above. In brief, grade I lesions are small and superficial and are located in noneloquent areas of the brain, while grade V AVMs are large and deep and found in functionally critical locations. Inoperable lesions are assigned to grade VI.
Degree of Confidence
With angiography, the degree of confidence is high. The presence of abnormal CNS vascularity is usually best accessed by using catheter angiography, which is considered the criterion standard for AVM detection. Nevertheless, catheter angiography is a useful adjunct to cross-sectional imaging in the overall assessment of CNS AVMs, and each test provides complementary information.
False Positives/Negatives
Angiographic false-positive findings are unusual but can occur in the presence of an early draining vein. This vein can be seen in a variety of disorders, typically a stroke. Abnormal neovascularity and abnormal venous drainage can also be seen in CNS neoplasms, particularly vascular glioblastomas and hemangioblastomas.
False-negative results can occur after an acute hemorrhage, when an AVM may become angiographically occult or compressed by an adjacent hematoma. Partially or totally thrombosed lesions may show less pronounced or absent AV shunting or may appear largely normal with a vascular-shift mass effect stagnant flow, which can further lead to a false-negative result.
INTERVENTION
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The treatment of an intracranial AVM typically involves 1 or more techniques including embolization, direct surgical or microsurgical resection, or radiosurgery. Usually, small or medium-sized AVMs located in noncritical areas of the brain can be removed successfully with conventional microsurgery. In contrast, large AVMs or AVMs in eloquent cerebral locations usually require staged, multimodal treatment.
Embolization
Occasionally, embolization is performed alone particularly when surgery is inadvisable or refused by the patient. The long-term goal of embolization is to reduce risk of cerebral hemorrhage, ultimately reducing the risk of overall morbidity and mortality from AVM rupture. AVM-related headaches often can improve after embolization alone, particularly when AV shunting ceases. When combined with surgery, embolization is performed to reduce the volume of the AVM nidus prior to surgical resection.
Smaller lesions have lower complication rates at surgery; therefore, they may not need preoperative embolization. Rarely, embolization may follow microsurgery, radiosurgery, or both (eg, when partial microsurgical resection yields a residual AVM that is too large for treatment with radiosurgery alone). A delay of 2-4 days to weeks between embolization and surgical resection may be beneficial, permitting vascular adaptation without allowing time for a major collateral supply to the AVM to mature.
Primarily, the agents used for AVM embolization include liquid adhesives, particles, and alcohol. Because particles alone usually are not considered a permanent embolic agent, polyvinyl alcohol (PVA) is typically used only in the preoperative setting. PVA particles have been used extensively in this capacity for more than 20 years. Advantages include their relative ease of use and favorable short-term histotoxicity. Among the shortcomings are an inability to fully permeate the AVM nidus and the need to use microcatheters that can be directed by guidewires, which have additional attendant risks. During embolization of a large AVM, a staged increase in particle size may be necessary. When flow in the AVM nidus has slowed significantly, final blockage can be achieved by using small microcoils.
Unlike particulate embolization, glue embolization with cyanoacrylates may allow a permanent and complete cure of AVM, though long-term follow-up studies have yet to demonstrate this definitively (see Images 21-22). Cyanoacrylates are a family of rapidly polymerizing adhesives, of which isobutyl-2-cyanoacrylate (IBCA) and N-butyl-2-cyanoacrylate (NBCA) are 2 members. Currently, many practitioners regard NBCA as the ideal embolic agent. Absolute alcohol can both obliterate aberrant vessels and penetrate capillary walls, causing destruction of normal cells. Accordingly, the use of glue or alcohol requires extreme care in the placement of the microcatheter tip.
The risk of major complications resulting from embolization is approximately 5-15%. Hemorrhage is a major risk because of inadvertent AVM rupture during the embolization procedure. Another problem is retrograde thrombosis leading to stroke. This can arise after successful occlusion of a major feeding artery if that artery is itself fed by a large trunk that supplies only a few other small normal branches. Then thrombosis may occur in the large trunk, with subsequent risk of infarct in the normal parenchyma supplied by the small branches. Thrombosis may also result from endothelial damage caused by the insertion of the catheter.
Inadvertent occlusion of nontarget vessels is a potential complication of any embolization procedure. Normal chronically hypoperfused vessels in the parenchyma surrounding the AVM may not be present during pre-embolization testing but remain at risk for inadvertent occlusion.
Normal perfusion pressure breakthrough (NPPB) is postulated to be another possible complication of AVM embolization resulting in cerebral hemorrhage, though the validity of the assertion is under debate. According to the theory, the small hemispheric vessels adjacent to an AVM must remain maximally dilated to divert blood from the lesion to normal brain parenchyma. Over time, the chronic dilatation leads to a loss of autoregulation, possibly at the arteriolar level.
When aberrant vessels of the AVM are occluded successfully during embolization, surrounding capillary beds may not be able to withstand the sudden exposure to normal perfusion pressure. Edema and or frank hemorrhage may result. Findings from some series suggest that NPPB may account for serious clinical complications in 1-3% of patients. Positive risk factors for NPPB are believed to include size, high flow, scanty filling of adjacent normal vasculature, steal from the vertebrobasilar or contralateral carotid circulations, excessive contribution to the nidus from the external carotid artery, and clinical findings of progressive or fluctuating neurologic deficit.
A large vein that drains both an AVM and normal structures may undergo thrombosis following occlusion by embolization of an AVM blood supply because arterial occlusion results in decreased venous blood flow. Venous infarct may occur in the normal territory.
Radiosurgery
Focused radiosurgery may be performed alone or in conjunction with other treatment modalities. Details are beyond the scope of this review; however, the advantages of radiosurgery include a high obliteration rate, particularly with small or medium-sized lesions, a low morbidity rate, and the lack of a need for general anesthesia. The radiosurgical obliteration rate is significantly lower with larger AVMs. Other disadvantages to radiosurgery include the 1- to 4-year latency period required for complete obliteration to occur and the risk of radiation-related white matter changes or vasculopathy.
Microsurgical resection
Microsurgical resection is the treatment of choice for small AVMs in noncritical areas of the brain. For AVMs in critical regions, microsurgery may provide immediate and permanent cure of the lesion and relief of symptoms. However, microsurgery also poses risks related to the use of general anesthesia but also the risk of creating 1 or more new neurologic deficits. Therefore, potentially curative embolization has gained in popularity in the definitive treatment of AVMs, small or large.
Patient age is another important consideration in the decision to perform surgery. Because the incidence of hemorrhage is highest in younger age groups, conservative treatment is often recommended for elderly patients. Other risk factors include the size and location of the AVM. Therefore, the Spetzler-Martin system is commonly used to predict the overall surgical outcome.
MULTIMEDIA
Section 11 of 12 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic
* Authors and Editors
* Introduction
* Differentials
* Radiograph
* CT SCAN
* MRI
* Ultrasound
* Nuclear Medicine
* Angiography
* Intervention
* Multimedia
* References
Media file 1: Brain, arteriovenous malformation (AVM). CT scan of the head demonstrates a left occipital AVM with multiple calcified phleboliths and numerous hyperattenuating vascular channels.
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Media type: CT
Media file 2: Brain, arteriovenous malformation (AVM). Axial T2-weighted MRI shows numerous flow voids corresponding to the CT findings (not shown). Note the mass effect on the lateral ventricle despite the lack of a mass or hemorrhage.
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Media type: MRI
Media file 3: Brain, arteriovenous malformation (AVM). Sagittal T1-weighted MRI demonstrates a large occipital AVM with parasagittal flow voids.
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Media type: MRI
Media file 4: Brain, arteriovenous malformation (AVM). T2-weighted coronal MRI.
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Media type: MRI
Media file 5: Brain, arteriovenous malformation (AVM). Diffusion-weighted MRI shows lack of signal intensity associated with an AVM.
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Media type: MRI
Media file 6: Brain, arteriovenous malformation (AVM). Lateral left carotid angiogram demonstrates a mixed pial-dural AVM. Arterial and occipital arterial feeders extend to the nidus via distal branches of the middle cerebral artery.
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Media type: X-RAY
Media file 7: Brain, arteriovenous malformation (AVM). Anteroposterior right carotid angiogram shows left, anterior, cerebral artery supply secondary to vascular steal. Note that the left anterior cerebral artery does not opacify with an ipsilateral carotid injection of contrast material (see also Image 6).
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Media type: X-RAY
Media file 8: Brain, arteriovenous malformation (AVM). Lateral left vertebral angiogram demonstrates a huge, left posterior cerebral artery feeder to the nidus.
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Media type: X-RAY
Media file 9: Brain, arteriovenous malformation (AVM). Anteroposterior left vertebral angiogram.
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Media type: X-RAY
Media file 10: Brain, arteriovenous malformation (AVM). Venous phase of a vertebral angiogram demonstrates numerous superficial and deep draining veins.
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Media type: X-RAY
Media file 11: Brain, arteriovenous malformation (AVM). Sagittal T1-weighted MRI shows a small, right parietal AVM with superficial venous drainage.
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Media type: MRI
Media file 12: Brain, arteriovenous malformation (AVM). T2-weighted axial MRI shows flow voids.
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Media type: MRI
Media file 13: Brain, arteriovenous malformation (AVM). Diagnostic angiogram obtained with a carotid injection shows the distal anterior cerebral artery (pericallosal artery) feeder, with superficial venous drainage to the superior sagittal sinus.
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Media type: X-RAY
Media file 14: Brain, arteriovenous malformation (AVM). Vertebral-injection image shows collateral arterial supply stemming from the distal posterior cerebral artery vessels.
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Media type: CT
Media file 15: Brain, arteriovenous malformation (AVM). Venous-phase image demonstrates large, superficial draining veins.
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Media type: Image
Media file 16: Brain, arteriovenous malformation (AVM). CT image of the posterior fossa demonstrating a hemorrhage in the fourth ventricle, with extension to the left cerebellum.
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Media type: CT
Media file 17: Brain, arteriovenous malformation (AVM). Axial T2-weighted MRI shows abnormal vascular flow voids along the left cerebellar tentorium.
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Media type: MRI
Media file 18: Brain, arteriovenous malformation (AVM). Left carotid angiogram demonstrates feeders to the dural malformation via the posterior division of the middle meningeal artery and occipital arteries.
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Media type: X-RAY
Media file 19: Brain, arteriovenous malformation (AVM). Left vertebral angiogram demonstrates small dural arterial feeders via posterior meningeal arteries, which arise directly from the vertebral artery.
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Media type: X-RAY
Media file 20: Brain, arteriovenous malformation (AVM). Venous-phase image demonstrates a venous aneurysm that projects inferiorly from cerebellar tentorium, the presumed cause of the patient's hematoma.
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Media type: X-RAY
Media file 21: Brain, arteriovenous malformation (AVM). Lateral left carotid angiogram in a patient with seizures with an unruptured left parasagittal AVM.
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Media type: X-RAY
Media file 22: Brain, arteriovenous malformation (AVM). Lateral left carotid angiogram obtained after successful staged embolization with a liquid adhesive shows lack of arterial venous shunting.
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