Medical Imaging of Cerebrovascular Disease Unit 3: Diagnostic Imaging |
The following are the imaging modalities that are used in the evaluation and diagnosis of cerebrovascular disease. In the diagnosis of stroke there is not one procedure that is 100% accurate for all types of the disease. Instead, a modality, or combination of modalities, may be chosen for the compatibility of diagnostic strengths with the nature of the patient's condition. Each topic area will include a description of the modality, its role in the diagnosis of stroke, and the strengths and limitations associated with each. |
Computed Tomography (CT) |
Fig. 3.1 (Click to enlarge) Non-contrast CT image showing extensive right sided intracranial hemorrhage in 81 year old male patient. Fig. 3.2 (Click to enlarge) Non-contrast CT image showing extensive right cerebral hemisphere infarction as darkened area of decreased detail in 86 year old male patient suffered RICA occlusion. Study was done one week post onset. Notice slight midline shift toward the left due to edema of infarcted area. Bright structures are non significant calcification of pineal gland (center) and choroid plexi (lateral). |
Non-contrast CT is the modality of choice in identifying stroke as either ischemic or hemorrhagic,3 and should be done as early as possible in order to begin anticoagulation (heparin) therapy and to maintain the option of thrombolytic therapy within the first three hours of onset. Intracranial hemorrhage is immediately evident as a hyperintensity within the hyperacute (< 6 hours) and acute (6-24 hours) periods, with subarachnoid hemorrhage almost as well detected.7 In cases of aneurysmal SAH, CT is effective at evaluating the size and location of the bleed, and can indicate the possibility of associated vasospasm, the presence of communicating hydrocephalus, and possibly identify the vessel of origin.6 Absence of evidence of hemorrhage correlated with clinical symptoms indicates ischemic stroke instead, and CT is sometimes able to detect subtle signs of diffuse swelling associated with large area of infarction, although not as reliably as MRI.4, 5 CT angiography (CTA) involves helical (spiral) scanning of the brain during an extended injection of intravenous contrast media, and is an important adjunct in the imaging of carotid stenosis and intracranial aneurysms. CTA has shown 92% correlation with angiography in determining the degree of carotid stenosis, with up to 100% in identifying surgical lesions.2 Its accuracy may be limited, however, in the presence of calcified plaques.2 In the evaluation of cerebral aneurysms, CTA has the advantages of being able to demonstrate the aneurysm neck, identify the extent of intra-aneurysmal clot and/or calcification, and show the relationships of the anuerysm with adjacent vessels and bone.6 Reported accuracy of CTA diagnosis of aneurysms is 88%, compared to 89% with that of angiography, although it can be limited by the presence of venous or other surrounding structures that complicate accurate interpretation. Improper scanning parameters can also obscure small aneurysms.6 CTA also has the disadvantage of requiring intravenous contrast.2 A representative protocol for CTA of the brain includes a total of 2cc/kg (100-150cc) of 300 concentration nonionic contrast, injected at a rate of 2-3 cc/sec. A delay of 20 seconds from the start of the injection to the initiation of the scan provides optimal visualization of the carotid arteries.4, 6 |
Magnetic Resonance Imaging (MRI) Standard MRI is unable to reliably identify areas of ischemia or infarction in the acute stages of stroke,7 although edema of brain tissue due to infarction may be seen in some patients as as a wedge-shaped area of bright image enhancement on T2 weighted scans9. Currently, brain MRI is not routinely performed in acute stroke patients, since hemorrhagic stroke can be confirmed or ruled out with non-contrast CT, and confirmation of infarction with MRI will not alter the course of treatment.3 However, new techniques are being refined that will allow MRI to provide this capability. A recent innovation in MRI technique that shows great promise in the evaluation of ischemic stroke is diffusion weighted imaging (DWI). Ischemia causes a shift in the water balance between the intra- and extracellular environment in cerebral tissue. This results in an accumulation of sodium and water within the cell which results in a slowing of the normal rate of movement of water molecules (Brownian motion). DWI can immediately detect areas of slower motion, identifying the area of ischemia or infarction within 1 hour of onset.13 A recommended MRI protocol for imaging of acute stroke includes the following eight components: T1,T2, proton density, FLAIR, r/o bleed, DWI, apparent diffusion coefficient mapping (ADC), and perfusion imaging.7 Of these, DWI, ADC mapping and perfusion scanning are sensitive in demonstrating areas of infarction. DWI . In depth discussion of the technical aspects of each component is beyond the scope of this discussion, although a brief definition of each is included in the Glossary section of this program. Magnetic resonance angiography is a special application of MRI that produces images of the blood flow through a vessel by taking advantage of the differences between non-moving tissue and flowing blood. Although MRA has been shown to be more accurate than ultrasound (20% misdiagnosis rate for ultrasound vs. 5% misdiagnosis rate for MRA2), current recommendations are for its use as a complementary modality to carotid duplex sonography in the evaluation of carotid stenosis. When used in combination and with both modalities in agreement, studies have shown 100% detection of surgical carotid artery disease.1,2 There are currently four techniques of MRA in common use, which are time-of-flight (TOF), phase contrast (PC), multiple overlapping thin-section angiography (MOTSA), and contrast enhanced MRA. |
Fig. 3.3 (Click to enlarge) Cerebral aneurysm. Fig. 3.4(Click to enlarge) Multiple cerebral infarcts in 36 y/o male in right basal ganglion area and posterior parietal lobe. Fig. 3.5 (Click to enlarge) MRA of common carotid artery bifurcation. |
Fig. 3.6 (Click to enlarge) Carotid duplex 2D sonogram showing common carotid artery with jugular vein above. Fig. 3.7 (Click to enlarge) Color flow doppler image of above image (fig. 3.8). The slower flow will be blue, with the faster flow in yellow & red. Fig. 3.8 (Click to enlarge) . Fig. 3.9 (Click to enlarge) . Fig. 3.10 (Click to enlarge) . Fig. 3.11 (Click to enlarge) . |
Carotid duplex sonography is recommended as the screening modality of choice in suspected atherosclerotic disease of the carotid bifurcation.1 It is completely noninvasive, inexpensive, mobile, and diagnostically accurate to 70-90% in detecting significant carotid stenosis.2 The accuracy rate increases to 94% for detecting ulcerated lesions.1 As it is unable to penetrate the cranium, however, it is generally limited to the evaluation of extracranial vessels. Patients who have experienced a TIA or have an identified carotid bruit should have screening CDS. If the patient has suffered a stroke, CDS can help make the determination of carotid stenosis as cause. Amaurosis fugax, or loss of vision in one eye, can be caused by thromboembolus originating from an atherosclerotic carotid lesion, and should also be screened by CDS.12 The purpose of screening patients with carotid stenosis is to determine the course of treatment; either with conservative therapies and medications or with surgical carotid endarterectomy (CEA). The principal determining factor is the degree of stenosis. Patients with a luminal narrowing greater than 60-70% are generally considered for surgery, hence the importance of accurately evaluating the stenosis. Carotid duplex sonography combines real-time gray-scale ultrasound with Doppler evaluation of blood flow, thereby providing information of both the structural anatomy of a vessel and the physiological movement of the blood within. Anatomic information includes the size of the vessel lumen and the structure of the vessel wall. An increase in the size of the intima & media layers of the arterial wall beyond 0.8mm is an indicator of disease in areas of stenosis less than 50%.10 As the vessel lumen narrows with increasing stenosis (>50%), the flow velocity increases, becoming more detectable with Doppler. Velocity will continue to increase with increasing stenosis, until reaching the >95% stage, where flow velocity will drop suddenly as the narrowing nears occlusion. In addition to increased flow velocity within the stenosis, high velocity jets of flow are created immediately distal to the stenosis (poststenotic), which are readily demonstrated with color Doppler imaging.10 As discussed in Unit 1, stroke rates can be significantly reduced if surgical carotid endarterectomy is performed in appropriate patients. Because of certain pitfalls associated with CDS, it has not been accepted as reliable for surgical determination on its own, but is being combined with MRA, another noninvasive technique, for correlation. It is reported that the number of patients requiring conventional angiography can be reduced by 80% with no effect on patient outcomes when correlation between these two modalities exists.2, 10 The strengths of each modality in this case can overcome the associated limitations of the other. Common pitfalls and limitations in CDS include the following:
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Cerebral angiography has long been considered the "gold standard" of cerebrovascular imaging, but has always carried a certain degree of risk because of its invasive nature. Currently much of this risk is being avoided with advances in the accuracy and reliability of other less invasive modalities such as carotid duplex sonography (CDS), magnetic resonance angiography (MRA), and CT angiography (CTA), therefore the call for conventional angiography in the diagnosis of stroke is diminishing. In the evaluation of carotid bifurcation disease, angiography has been largely supplanted by the combination of CDS and MRA, and is called for only in cases of poor correlation between the two.2, 10 Angiography is still the procedure of choice, however, in evaluating intracranial aneurysms, as it is able to demonstrate the neck of the aneurysm, identify the presence of multiple aneurysms, vasospasm associated with SAH, and the presence of an AVM and its associated feeder vessels.11 Angiography is also finding an increasing therapeutic role with advances in neurointerventional techniques. The cerebral arteriogram is an invasive procedure that involves the placement by the physician of an arterial vascular catheter, usually into the femoral artery, that is directed through the abdominal and thoracic segments of the aorta until it reaches the aortic arch. It is then directed into the cerebral circulation via the brachiocephalic, left common carotid, or left subclavian arteries for the injection of contrast into selected vessels. The "four vessel" cerebral arteriogram will demonstrate the entire cerebral vascular anatomy via contrast injection into the right and left internal carotid arteries and vertebrobasilar circulation. Frontal and lateral projections are obtained, as well as various oblique projections when indicated. Most angiographic images in the modern special procedures department are high resolution digital, or 14"x14" cut film. This provides the highest spatial resolution of all the modalities. A detailed discussion of catheterization and procedural techniques is beyond the scope of this discussion. As previously mentioned, angiography is an invasive procedure with risks associated with two main areas, the catheter placement and manipulation, and the intravascular contrast media. Risks to the patient from placement and manipulation of the catheter include hemorrhage, injury to the artery from the needle puncture, injury to the part of the body supplied by the artery, emboli to the distal extremity (from the puncture site), emboli from accidental dislodging of atherosclerotic plaques in the aorta or branch vessels, stroke from dislodged plaque, air embolus introduced during the contrast injection, thrombus formed at the tip of the catheter, or death. Angiography carries a 1.2% incidence of carotid associated infarction (National Institute of Health Clinical Advisory, September 28, 1994).1 Risks to the patient from iodinated contrast media include all potential complications normally associated with the use of i.v. contrast. In addition, because of the concentrated bolus required for cerebrovascular imaging, neurologic complications, most commonly in the form of seizures, may occur. Keeping the amount of contrast media used to a minimum and using nonionic/low osmolar contrast agents reduces the risk of these complications.8 Angiography does have certain limitations. It can only demonstrate the lumen of the vessel, whereas other modalities are able to provide information about the vessel wall and the composition of a plaque or thrombus. Also, because it is essentially a two dimensional medium, at least two projections, often more, must be performed in order to profile an atherosclerotic lesion to accurately evaluate the degree of stenosis. The accurate demonstration of stenotic lesions is dependent on the proper orientation of the lesion with the radiographic projection, therefore a stenosis may be overestimated or underestimated.1 However, the new technique of rotational angiography can overcome much of this type of problem.6 |
Fig. 3.12 (Click to enlarge) Patient with right sided hemiparesis from left sided embolic stroke . The central depression in the atheromatous plaque in the ICA at the carotid bifurcation indicates ulceration, a favorable site for clot formation. A subtle filling defect on the superior aspect of the plaque indicates the tail of accumulated thrombus, the most likely source of the patient's stroke. Notice delayed or absent filling of the MCA branches of the Sylvian triangle, identifying site of occlusion. Fig. 3.13 (Click here for additional images and explanation.) Giant berry aneurysm arising from the distal ICA. The hemispherical contrast filled vascular enlargement at the terminus of the left internal carotid artery is a giant "berry" aneurysm, arising from the internal carotid artery. Notice the incomplete filling of the aneurysm resulting from the patient being supine with the heavier contrast filling the most dependent portion of the sac. Notice also the nasogastric & endotracheal tubes in place, indicating the critical nature of the patient's condition. Fig. 3.14 (Click to enlarge) Cerebral AVM. |
Fig. 3.15 (Click to enlarge) Arteriography subtraction image of giant parietal lobe AVM arising from the middle cerebral artery. Fig. 3.16 (Click to enlarge) MRI image of an occipital lobe AVM, identified by the dark "w"-shaped vessel coursing through the cerebral tissue superior to the cerebellum. In this image, the vessel is dark due to the absence of signal detection from the flowing blood. Fig. 3.17 (Click to enlarge) Arteriography subtraction image of aneurysmal avm. |
Cerebral Arteriovenous Malformations (AVM's) The cerebral arteriovenous malformation (AVM) is not generally considered as a cause of stroke per se, because of the differences in etiology between the two; stroke being mainly an acquired condition associated with aging, and the AVM a congenital condition seen in younger individuals. However, AVM's produce similar neurological symptoms, and are diagnosed and treated in much the same way, therefore a discussion of cerebrovascular disease is incomplete without considering them. An AVM is a tortuously dilated collection of abnormal vessels characterized by multiple enlarged feeder arteries and dilated venous outflow vessels, resulting in rapid flow of blood through the vessels. The accelerated blood flow produces three pathological conditions. Blood is shunted away from normal brain tissue, resulting in inadequate blood supply. Because the flow is rapid and the vessels are enlarged, hemorrhage is a frequent occurance. Neurological deficits may result from the mass effect of the growing lesion on adjacent brain structures. The symptoms produced by these factors include severe headache, seizures, and progressive neurological deficits.11 Cerebral AVM's occur due to congenital abnormal development of the cerebral vasculature. Structurally, the abnormal vessels have characteristics of both arteries and veins. As these structures have a tendency to enlarge, they vary in size. Secondary conditions that may occur include thrombosis, calcification and thrombosis.11
Most AVM's become symptomatic during the second and third decades of life. 80% are manifest before age 40. 10% of intial bleeds are fatal, while 30% produce some degree of disability.11 Screening imaging modalities commonly used in the diagnosis and evaluation of AVM's are CT, MRI, and MRA, with confirmation and surgical evaluation by angiography. In order to help determine the course of treatment, information must be obtained about the location, size, and the number of feeder vessels of the AVM. MRA has shown particular promise as a non-invasive modality because of its ability to demonstrate the nidus of the AVM as well as delineate multiple feeder arteries and draining veins15. Surgery carries low risks of mortality and morbidity if the AVM is small. Most small AVM's are resected unless they are located in the vital areas of the brain stem or basal ganglia. For those located in non-surgical areas, radiotherapy of at least 2500 rads can effectively reduce the AVM and alleviate symptoms. However, this is not a viable option with AVM's larger than 3cm. due to increasing risk to healthy tissue and less effectiveness in reducing the lesion. The most attractive option for large AVM's is selective transcatheter embolization. This involves placement of a small calibre "microcatheter" as close as possible to the nidus of the AVM, and the injection of an embolic material to induce thrombosis. Materials currently used for embolization include Ivalon, detachable balloons, coils, and methylacrylate glue.11,13,14 Less frequently occuring types of AVM's are telangectasias, cavernous angiomas, venous angiomas, and vein of Galen aneurysms.11 |
REFERENCES
1. Anton, R., "A Common Sense Approach to Diagnostic Imaging of Carotid Vascular Disease", Applied Radiology, July 1997. |
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Images and text copyright Ken McCormick, April 1999. All rights reserved.