eMedicine Specialties > Radiology > Brain/Spine
Brain, Arteriovenous Malformation: Imaging
Updated: Dec 31, 2008
Radiography
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 the clinician to order cross-sectional imaging.15,17,18,19,20
Degree of Confidence
The 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 for the detection of AVMs of the CNS.
Computed Tomography
Findings
CT scanning of AVMs of the brain can show an isoattenuating-to-hyperattenuating hemispheric mass, as well as detect an accompanying abnormal vascular supply. In the absence of hemorrhage, nonenhanced CT scanning can demonstrate small foci of calcification in as many as 30% of patients (see Image below and Image 1 in Multimedia). Other possible findings include cystic cavities representing previous hemorrhage and hypoattenuation of surrounding parenchyma representing encephalomalacia, cerebral atrophy, or gliosis.
A CT scan of the head that demonstrates a left occipital arteriovenous malformation (AVM), with multiple calcified phleboliths and numerous hyperattenuating vascular channels.
Contrast-enhanced CT scanning can demonstrate serpiginous vascular enhancement that is uniquely typical of an AVM. Occasionally, CT scans can demonstrate edemas, mass effect, or ischemic changes that may be associated with AVMs, and further contrast-enhanced imaging may identify small AVMs missed by plain CT examination.
In the hyperacute stage of hemorrhage, a pial AVM appears as a hyperattenuating parenchymal lesion on nonenhanced CT scans 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 concomitant 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 that progresses to normal brain parenchyma. Nonenhanced lesions viewed during the isoattenuating phase may therefore 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 as a hypoattenuating area 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 scanning.
In an emergency setting, CT scanning can show a presenting cerebral or extra-axial hemorrhage. CT scans may show secondary signst that infer the presence of a dural AVM (ie, abnormal enlarged dural sinuses or draining cerebral veins). Typically, these are best appreciated using contrast imaging. Unfortunately, the dural malformation nidus is typically poorly demonstrated on CT scans alone.15
Degree of Confidence
The degree of confidence is moderate with CT. Typically, an additional study, such as MRI or catheter angiography, is necessary to confirm the presence of an AVM; however, 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 are associated with CNS calcifications, which can lead 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. Furthermore, an AVM may be overlooked if it is compressed by an adjacent parenchymal hemorrhage. Lastly, vascular AVMs may be misconstrued as cerebral hemorrhage because of the presence of large hyperattenuating vessels. Contrast-enhanced CT scanning or supplemental MRI or MRA can help clarify difficult cases.
Magnetic Resonance Imaging
Findings
MRI findings
On MRI, a typical unruptured AVM appears as a tightly packed or loose tangle of vessels (see Image below and Image 2 in Multimedia).
Arteriovenous malformation (AVM) of the brain. An axial T2-weighted MRI showing 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.
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 AVMs.
MRI scans can show the lesion size and, usually, the primary supply of the AVM and its venous drainage. MRI can further demonstrate associated aneurysms on arterial feeders as well as 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 abnormally reduced signal intensity on T1-weighted images and increased signal intensity on T2-weighted, proton density—weighted, and short-tau inversion recovery (STIR) 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 appears 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 appears hyperintense on both T1- and T2-weighted imaging, which is consistent with the presence of methemoglobin. Chronic hematoma is characterized by a central hyperintense core surrounded by a ring of hypointensity resulting from 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 for detecting aneurysms smaller than 1-2 cm is low.15
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 best performed 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.15
Magnetic resonance angiography
MRA is a noninvasive alternative to conventional angiography. Certain lesions hidden on conventional angiograms may be identified only on MRI scans 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. Flip angles of approximately 15º and a repetition time (TR) of 40 ms are usually 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, such as velocity encoding (V enc) = 20 cm/s. Otherwise, imaging with V enc of 80-100 cm/s typically demonstrates the arterial supply. Complex flow in the AVM nidus is best seen on 3D TOF acquisitions, using small voxel size, partial echo sampling, and a short echo time (TE).14,15,16,21
Degree of Confidence
The degree of confidence is high with MRI. MRI scans 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; these include cavernous angiomas, venous angiomas, and capillary telangiectasias. Lesions are associated with a lower risk of rupture, but they can mimic the appearance of an AVM; however, they lack characteristic AV shunting. Nevertheless, false-positive findings may prompt catheter angiography for clarification. MRI scans can also show abnormally enlarged arteries (atriomegaly), a finding which is suggestive of an underlying malformation when none is present.
False-negative MRI findings of CNS AVMs can occasionally 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.
Ultrasonography
Findings
Ultrasonography is not typically used for evaluating cerebral AVMs. Ultrasonography may play an adjunctive role during open neurosurgery for the purposes of AVM localization.15
Nuclear Imaging
Findings
Isotopic cerebral blood flow studies have largely been supplanted by modern CT scanning, MRI, and digital subtraction angiography of the brain for the evaluation of AVMs.21
Single-photon emission CT (SPECT) and positron emission tomography (PET) of the brain are useful for imaging ischemic penumbra surrounding a vascular lesion. Furthermore, these studies may be helpful in the functional imaging of normal parenchyma surrounding a vascular malformation. This discussion is currently beyond the scope of this article.15
Angiography
Findings
Conventional cerebral angiography is the criterion standard for the evaluation of AVMs (see Images below and Images 6-10 in Multimedia). 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).
A lateral left carotid angiogram demonstrating a mixed pial-dural arteriovenous malformation (AVM). Arterial and occipital arterial feeders extend to the nidus via distal branches of the middle cerebral artery.
Arteriovenous malformation (AVM) of the brain. An anteroposterior right carotid angiogram showing 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).
Arteriovenous malformation (AVM) of the brain. A lateral left vertebral angiogram demonstrating a huge left posterior cerebral artery feeder to the nidus.
Arteriovenous malformation (AVM) of the brain. An anteroposterior left vertebral angiogram.
Arteriovenous malformation (AVM) of the brain. The venous phase of a vertebral angiogram that demonstrates numerous superficial and deep draining veins.
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 they are supplied by dural vessels, such as the meningeal branches or occipital arteries of the external carotid arteries, or the meningeal branches of the internal carotid or vertebral arteries.
Catheter angiography can usually 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 the angiographic data described above. In brief, grade I lesions are small, superficial, and located in noneloquent areas of the brain, whereas grade V AVMs are large, deep, and found in functionally critical locations. Inoperable lesions are assigned to grade VI.9,15,21
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 (most typically, in 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 they may appear largely normal, with a vascular-shift mass effect stagnant flow; this can further lead to a false-negative result.22
More on Brain, Arteriovenous Malformation |
| Overview: Brain, Arteriovenous Malformation |
 Imaging: Brain, Arteriovenous Malformation |
| Multimedia: Brain, Arteriovenous Malformation |
| References |
| « Previous Page | Next Page » |
References
De Biase L, Di Lisi F, Perna S, Spalloni A, Ferranti F, Lucani A, et al. Recurrent episodes of syncope in a patient with cerebral arteriovenous malformation. Clin Ter. Mar-Apr 2007;158(2):147-50. [Medline].
Barrow DL. Intracranial Vascular Malformations. Park Ridge, Ill: American Association of Neurological Surgeons; 1990.
Jafar JJ, Awad IA, Rosenwasser RH, eds. Vascular Malformations of the Central Nervous System. Philadelphia, Pa: Lippincott, Williams & Wilkins; 1999.
Toole J, Murros K, Dindagur N. Cerebrovascular Disorders. 5th ed. Philadelphia, Pa: Lippincott-Raven; 1999.
Yamada S, ed. Arteriovenous Malformations in Functional Areas of the Brain. Armonk, NY: Futura Publishing Company; 1999.
Kase CS, Caplan LR. Intracerebral Hemorrhage. Boston, Mass: Butterworth-Heinemann; 1994.
Olesen J, Welch KM, Tfelt-Hansen, eds. The Headaches. 2nd ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 2000.
Tsutsumi M, Aikawa H, Kodama T, Iko M, Nii K, Matsubara S, et al. Symptomatic inferior cavernous sinus artery aneurysm associated with cerebral arteriovenous malformation. Neurol Med Chir (Tokyo). Jun 2008;48(6):257-8. [Medline].
Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg. Oct 1986;65(4):476-83. [Medline].
Wang HU, Chen ZF, Anderson DJ. Molecular distinction and angiogenic interaction between embryonic arteries and veins revealed by ephrin-B2 and its receptor Eph-B4. Cell. May 29 1998;93(5):741-53. [Medline].
Graham DI, Lanton PL. Greenfield's Neuropathology. New York, NY: Arnold Publishers; 1997.
Spetzler RF, Wilson CB, Weinstein P, Mehdorn M, Townsend J, Telles D. Normal perfusion pressure breakthrough theory. Clin Neurosurg. 1978;25:651-72. [Medline].
Grossman RG, Loftus CM, eds. Principles of Neurosurgery. 2nd ed. Philadelphia, Pa: Lippincott-Raven; 1999.
Anderson CM, Edelman RR, Turski PA. Clinical Magnetic Resonance Angiography. New York, NY: Raven Press; 1993.
Orrison W Jr. Neuroimaging. Vol. 1. Philadelphia, Pa: WB Saunders Co; 2000.
Potchen EJ, Haacke EM, Siebert JE, Gotschalk A. Magnetic Resonance Angiography Concepts and Applications. St Louis, Mo: Mosby-Year Book; 1993.
Baum S. 1997. In: Abram's Angiography: Vascular and Interventional Radiology. Vol 1. Philadelphia, Pa: Lippincott-Raven.
Baum S, Pentecost M, eds. Abram's Angiography: Interventional Radiology. Vol. 3. 4th ed. Boston, Mass: Little, Brown & Company; 1997.
Connors JJ, Wojak JC. Interventional Neuroradiology. Philadelphia, Pa: WB Saunders Co; 1999.
Osborn AG, Tong KA. Handbook of Neuroradiology: Brain and Skull. 2nd ed. St. Louis, Mo: Mosby-Year Book; 1996.
Hadizadeh DR, von Falkenhausen M, Gieseke J, Meyer B, Urbach H, Hoogeveen R, et al. Cerebral arteriovenous malformation: Spetzler-Martin classification at subsecond-temporal-resolution four-dimensional MR angiography compared with that at DSA. Radiology. Jan 2008;246(1):205-13. [Medline].
Codd PJ, Mitha AP, Ogilvy CS. A recurrent cerebral arteriovenous malformation in an adult. J Neurosurg. Sep 2008;109(3):486-91. [Medline].
Further Reading
Keywords
AVM, arteriovenous malformation, AV malformation, arteriovenous malformations, vascular malformation, AVM brain, arterial venous malformation, arteriovenous aneurysm, arteriovenous angioma, cerebrovascular malformations, pial AVMs, parenchymal AVMs, dural AVMs, vein-of-Galen aneurysm
