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Diffusion-weighted magnetic resonance imaging (MRI), ce-rebral perfusion,computed tomogrsupplement standWhile beneficialwhen caring forinfarction, the mucate the patientsscribe the basicsfor a patient wittheir utility, andfindings.

NONCONTRASTDue to its broadCT is considered the first line of imaging of patients with

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brain is per-l neurologicontraindica-us thrombo-

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appears (eg, bone or calcium), while less dense material isdarker (eg, air in the sinuses). Acute blood has the fortunate

plexus.If the patient presents with a new-onset focal neurologic

deficit, and the CT reveals an intracranial hemorrhage, ob-

ment of Medical Imaging, Division of Neuroradiology, University ofArizona Medical Center, 1501 North Campbell Avenue, Tucson, AZ85724.

E-mail address: rkhan@radiology.arizona.edu

0002-9343/$ -see front matter 2013 Elsevier Inc. All rights reserved.http://dx.doi.org/10.1016/j.amjmed.2012.11.014imaging property of being higher density than normal brain,so it is very conspicuous on the noncontrast CT. Incidentalcalcifications that may be mistaken for hemorrhage mayoccur in the globus pallidus, pineal gland, and the choroid

Funding: None.Conflict of Interest: None.Authorship: All authors had a role in writing the manuscript.Requests for reprints should be addressed to Rihan Khan, MD, Depart-and noninvasive angiography using bothaphy (CT) and MR are widely available toard imaging techniques of MRI and CT.to patient evaluation and management,a patient with a potential acute cerebralltitude of diagnostic options may compli-imaging evaluation. This article will de-

of imaging studies that may be performedh a potential cerebral infarction, explaindiscuss the significance of the imaging

HEAD CTavailability and speed, noncontrast brain

tuting therapy.To this end, a noncontrast CT scan of the

formed to look for other causes of the new focadeficit besides ischemic disease and for any ctions to therapy. The goal is to start intravenolytic therapy in patients with clinical suspicionischemia without any contraindication. MRI issitive imaging modality than a noncontrast CTdetection of early infarction; however, becausequicker and much more readily available, CT ithe first study in most centers.

The CT scan is done without contrast, becaenhancing lesion may be mistaken for an intraorrhage. On CT, the denser the material is, tcute Stroke Imaging: Whatan Khan, MD, Kambiz Nael, MD, William Erly, MD

partment of Medical Imaging, Division of Neuroradiology, Unive

ABSTRACT

Advances in technology and software applicationstrategies in the evaluation of patients with susptomography (CT) and magnetic resonance imaginimaging, which have been complemented by CT anand cerebral perfusion studies, while conventionaltherapy. The purpose of this article is to review the vsetting, and to discuss the utility of each and the peof which study and when each should be ordered isreader should have a more clear understanding of thimaging. 2013 Elsevier Inc. All rights reserved. The AmKEYWORDS: Acute stroke; CT stroke; MRI stroke; Stro

vances in technology and neuroscience have contributednew neuroimaging modalities and strategies in the eval-tion of patients with suspected acute cerebral infarction.icians Need to Know

f Arizona Medical Center, Tucson.

contributed to new imaging modalities andacute cerebral infarction. Routine computedI) have been the standard studies in stroke

angiography, diffusion-weighted MR imaging,graphy is typically reserved for intra-arterialof imaging studies available in the acute strokeassociated main findings. The appropriatenessiscussed. At the conclusion of this article, theoimaging modalities available for acute stroke

Journal of Medicine (2013) 126, 379-386oke imaging

pected acute stroke in many centers across the country.cause intravenous tissue plasminogen activator (tPA) isfirst-line therapy for acute ischemic infarction, potential

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380 The American Journal of Medicine, Vol 126, No 5, May 2013usly they are not a candidate for thrombolysis. If nood is seen on the noncontrast CT, an intracranial hem-hage is excluded, but ischemic disease is still in theferential diagnosis. Early on in the course of an ischemicarct, the head CT scan may look normal. Signs of earlyarction that may indicate anly ischemic stroke include:

the insular ribbon sign;the basal ganglia sign;global loss of gray-white differ-entiation;mild sulcal effacement; andthe dense middle cerebral artery(MCA) or dense basilar arterysign.

A brief digression into theysical principles that are re-nsible for the changes in thescan as a result of ischemic

ease will make understandingsigns of early infarction easier.e of the first concepts to re-mber is that water (serum) iss dense than cellular materialdily confirmed comparing theebrospinal fluid (CSF) in the

ntricles to the surroundingin. As a result of hypoperfusion, cellular oxidative me-olism decreases or completely stops, rendering the cellable to produce adenosine triphosphate (ATP). ATP-de-ndent membrane transport terminates and the net effect ister being drawn into and becoming trapped within thel. As the cellular water content increases, the CT densitythe affected tissues decreases, in a type of visual aver-

ing of the normal brain parenchyma with the black CSF.e insular ribbon sign (Figure 1A) results from edemasing a loss of gray-white differentiation within the insu-cortex. This region is sensitive to early ischemic disease.alogous to the insular ribbon sign is the basal ganglian (Figure 1B) in which there is edema of the globusllidus, putamen, or caudate nucleus, and a loss of visual-tion of these structures. In the case of a large or slightlyer infarction, one may see a loss of gray-white differen-

tion throughout the affected area (Figure 1C). This isquently associated with effacement of the adjacent sulci,ich is reflective of the cellular edema and development ofld regional mass effect.In contrast to the decreased density of the affectedas of the brain described previously, the dense MCA

igure 2A) or dense basilar artery signs are areas ofnormal increased density within the vessel lumen. Theh density corresponds to thrombus lodged within theery and has been shown to occur in up to one third toe half of patients with angiographically proven throm-

CLINICAL SIGNIFI

In acute stroke, finial hemorrhage, athrombolysis.

Cervical and cereevaluated with co(CT) or magneticgiography to lookstenosis, dissectioand other vascular

Perfusion studies ceither CT or MR topenumbra and cor

Conventional angireserved for intra-sis.1,2 It is therefore useful when seen, but CT is not siofficiently sensitive to exclude a proximal thrombus ifdense vessel is not seen.

After around 6 hours, ischemic tissue becomes moreiably visibly evident as the affected tissue becomes moreematous. Studies have shown that the area of hypodensity

seen on noncontrast CT correlateswith infarcted tissue. When eval-uating the CT scan at presentation,when an MCA territory infarctionis suspected, it is important to ob-serve how much of the territory isinvolved, as involvement of 1/3of the MCA territory is associatedwith an increased risk of bleedwith thrombolysis,3 while in-volvement of 1/2 of the MCAterritory is associated with brainherniation.4 Hence, there is the con-traindication to tPA when more than1/3 of the MCA territory is involvedon noncontrast CT.

Mass effect from an infarctiontypically peaks around 3-5 days.Acute infarcts also may undergohemorrhagic conversion, which iscommonly thought to representreperfusion injury into severelyischemic tissue via recanalized ar-

ies or via collateral flow. Lastly, after weeks to months,infarct evolves to its chronic state (Figure 1D), when

ema is long gone and volume loss is clearly evidentcephalomalacia).

ANGIOGRAPHY OF THE HEAD AND NECKcerebral ischemia is suspected after the initial CT scan,aluation of the status of the neck and brain arterial vas-lature is recommended. CT angiography (CTA) is muchre readily available than magnetic resonance angiogra-

y (MRA), with diagnostic accuracy approaching that ofnventional angiography. A relatively small bolus of in-venous contrast is given, and with modern CT scanners,ombined CTA of the head and neck can be performed

th one contrast injection.Significant findings on the CTA of the neck includeh-grade arterial stenosis (Figure 2B), occlusion, or dis-tion. Plaque ulceration also may be seen from a rupturedque. In the intracranial vasculature, areas of stenosis and

clusion also may be seen, and sometimes the clinicalsentation points to an area of high clinical suspicion in a

rticular vascular territory. Focal areas of intraluminal clotbe seen outlined by contrast, in the form of either

erial stenosis or complete occlusion (Figure 2C). CTAs been shown to be sensitive for detection of intracranialombus in the large arteries, but not for the more distal,aller branches.4 Once identified, proximal branch occlu-

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381Khan et al Acute Stroke Imagingchanical thrombectomy, as opposed to intravenousombolysis, given that intra-arterial thrombolysis may bere efficacious in treating proximal large vessel occlusion

mpared with intravenous thrombolysis.5 The time fromset of symptoms to initiation of treatment also is a majortor, as intra-arterial thrombolysis and mechanical throm-

ctomy have longer window periods for treatment thanes intravenous thrombolysis. Less commonly, multifocal

Figure 1 Signs of early infarct comparedNotice the small focal area of low density inrelative to the posterior aspect (arrows). (B)low density throughout the right basal ganglleft basal ganglia maintain their normal higinfarct, left middle cerebral artery territory.with well-delineated borders. In this case, nobasal ganglia are not. (D) Chronic infarct in lfrom cerebrospinal fluid replacing the infarcventricle. An acute to subacute ischemic inalso is seen on the right side.as of arterial narrowing may suggest vasculitis, but this strgnosis can be more sensitively assessed in the clinicalntext of systemic disease.Besides visualizing the arterial vasculature, the CTArce images (CTA-SI) are very useful as they reflectod volume.5 With contrast, normal brain tissue will en-

nce while areas of infarction will not, thus making thearcted tissue more apparent, even more than on the con-rrent noncontrast head CT. Size of the infarct as demon-

hronic infarct: (A) Insular ribbon sign.terior portion of the insular gray matterganglia sign. Notice the subtle uniformll arrows), while the gray nuclei of thensity (large arrows). (C) Acute large

ubtle loss of gray white differentiationw the insular ribbon is involved, but theietal lobe (arrow). Note the low densityin and dilation of the ipsilateral lateralat underwent hemorrhagic conversiondiaco

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382 The American Journal of Medicine, Vol 126, No 5, May 2013e of infarct on follow-up CT.4 CTA-SI has been shown tocomparable to diffusion-weighted imaging (DWI) in the

tection of ischemic regions, with DWI better at detectingall infarcts and those in the brainstem and posteriorsa.6,7Pitfalls to watch for include a suboptimal contrast bolus,ich may warrant a repeat examination, and significant

nous contamination. Also remember that vascular con-st may have a nephrotoxic effect. Radiology departmentsuld have a protocol in place for how to deal with contrast

ministration in the setting of poor renal function. Alter-tively a noncontrast MRA could be performed to evaluate

head and neck, or an ultrasound examination to evaluatecarotid bifurcations.

PERFUSIONCT perfusion study can be performed to look for ischemiainfarct, as the clinical neurologic examination cannotferentiate the nonfunctioning reversibly ischemic tissuem irreversibly infarcted tissue. This can be done at thee time as a CTA study by adding a second contrast bolus

d repeating the scan, tracking changes in cerebral en-ncement over time. This allows for assessment of thehemic penumbra, which is the area of potentially salvage-le tissue ischemia surrounding an area of core infarct.Although more maps are now available, the key basic

rfusion maps to focus on are: cerebral blood volumeBV), cerebral blood flow (CBF), and mean transit timeTT). The key to understanding these maps is an under-

igure 2 Vascular abnormalities to look for: (A) Dense middle cegment related to clot. This density was focal and significantly brimporal subacute infarct. (B) Severe stenosis. Computed tomogra

tenosis at the origin of the left internal carotid artery related to athformatted image from head CTA shows an abrupt cutoff of the more distal branches is related to collateral flow.nding of the physiologic principals of ischemia and in- scaction. Ischemic brain has reduced blood flow and there-e it takes longer for the blood to get through the affectedin (Figure 3), resulting in decreased CBF and increasedT. CBV remains near normal in ischemic brain becausetill has some blood flowing through it, which is enoughkeep the tissue alive but not enough for normal function.Like ischemic brain, the infarcted brain will have anvated MTT and decreased CBF. The distinguishing fea-e that allows differentiation of ischemic brain from in-cted brain is the CBV: there is no blood volume in thearcted brain.The color assignments regarding increased and de-ased flow vary from center to center. A color scale isnted along the side of the images to indicate what colorsresent increased or decreased flow, transit time, or vol-e. Symmetry is key to interpretationif the examination

symmetric on all 3 maps, either the examination is nor-l, or there are bilateral symmetric areas of ischemia orarction.A major pitfall with CT perfusion with most current CTnners is that the entire brain is not scanned during thedy. Even with a 64-slice CT scanner, only 4 or 5 slices

typically obtained, centered at the level of the basalnglia where the anterior, middle, and posterior cerebralscular territories can be assessed. If a small infarct issent in an area of the brain that was not imaged, it willmissed. Some people therefore advocate repeating thedy at a different location. Alternatively, techniques haveen devised to move the table back and forth during the

l artery sign. High density is present in the proximal right M1han the other arteries. Also note the areas of right frontal andgiography (CTA) coronal reformatted image shows a severerotic plaque build-up (arrow). (C) Arterial occlusion. Coronaldistal left M1 segment (arrow). Contrast opacification of theto

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383Khan et al Acute Stroke Imagingscanners can scan the entire brain without moving thele (320 slices), but they are not yet prevalent. Consider-on also must be given to patients with preexisting diseased infarct, brain tumor); the perfusion study will be alteredd one must take care to consider this when evaluating theps. As with CTA, because contrast is given, renal func-n should be considered.

II may be performed after any of the previously dis-

ssed CT scans, and in some instances may be the firstaging test performed. In evaluation of suspected cerebralarction, the key sequence to be familiar with is DWI.cause this image set is a map of water motion, when theP-dependent membrane pumps stop working in infarctedin, water becomes trapped within the cell, resulting inch higher signal than from the background tissues.metimes, areas that are bright on T2-weighted imagesth normal diffusion properties will show up as relativelyh signal areas on the DWI (a phenomenon known as T2ne-through). The high signal area on the DWI must berrelated with the finding on the apparent diffusion coef-ient (ADC) map. Acute infarct will appear dark on theC map, confirming restricted diffusion. So the overall

ttern to look for is: bright on DWI, dark on ADC (Figure, B). It also is important to remember that not everythingt shows restricted diffusion represents acute infarction.r example, pyogenic abscesses and highly cellular neo-sms also may show restricted diffusion, so the clinical

ntext and the remainder of the imaging study need to beutinized.Because the ATP-dependent membrane pumps stop

igure 3 Computed tomography perfusion ischemia. Cerebraldecreased in a wedge-shaped area that is more blue in the left froTT) in the same area that is more red and yellow (C). Note the re

ero and red represents the maximum value of the scale. If this wererea as in the CBF and MTT maps.Figure 4 Magnetic resonance image (MRI) of acute infarct.(A) Bright signal on diffusion weighted imaging (DWI) withcorresponding matching low signal on the apparent diffusioncoefficient (ADC) map (B) indicates restricted diffusion fromacute infarct. This is the MRI that corresponds to the computedtomography (CT) scan in Figure 1C. (C) Coronal gadolinium-enhanced magnetic resonance angiogram from aortic arch tojust above the circle of Willis shows a proximal left middlecerebral artery occlusion (arrow). (D) Infarct underwent hem-rking nearly immediately, acute infarction will showoolume (CBV) map (A) is normal. Cerebral blood flow (CBF)ion (B) with corresponding prolongation of mean transit timee color scales to the side of each image, where blue represents

t, the CBV map would show a similar abnormal wedge-shapedrrhagic conversion by day 2 as shown on head CT scan.

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384 The American Journal of Medicine, Vol 126, No 5, May 2013tricted diffusion within 30 minutes of the initial event.e practical implication of this is that by the time anytient gets to the emergency department and placed in thenner, virtually everyone with an acute infarct shouldw changes on the DWI sequence. Why not go to MRIt? Some large institutions that have their MRI scannerse to the emergency department and have 24/7 in-house

technician coverage may do that to simply answer ifre is an infarct or not. However, often a noncontrast CTn is still performed to rule out a bleed because the high

nsity of blood makes its presence very recognizable on, and detecting acute hemorrhage on MRI can beficult.Infarcts will vary in shape and size, depending on thegree of arterial involvement. Proximal branch occlu-ns, such as the M1 segment of the MCA, can causearction of the entire MCA territory if there is notequate collateral circulation. Smaller, more down-eam branch occlusions will cause subterritorial in-cts, while tiny clots (as with embolic disease) willuse terminal branch occlusions and small associatedarcts. Embolic infarcts are suspected when infarctscur in more than one vascular territory: MCA, anteriorrebral artery, or posterior cerebral artery. Ultimately,en an infarct has evolved to the chronic stage, just asCT, there will be volume loss and encephalomalacia.

ter infarcted tissue is resorbed, CSF fills in the cavi-ed area that follows fluid signal intensity on MRI.Regarding the exclusion of intracranial hemorrhage inhyperacute stroke patient, MRI appears to be at least

ual to CT. Gradient-recalled-echo images can detectcrohemorrhages, both old and new, better than CT, andparticular, 5 microhemorrhages have not been shownbe a contraindication to thrombolysis. The fluid-atten-ted inversion recovery sequence can be used to detectbarachnoid hemorrhage, but may be associated withifacts at the skull base that mimic subarachnoidod.5 Hyperoxygenation also can cause high signalensity in the CSF spaces that mimics subarachnoidod.8Some contraindications to MRI include cardiac pace-ker, metal in the eye, inability to fit in the scanner, and anbility to stay still. The latter is particularly problematic inpatient with acute mental status change. Contrast is not

cessary for this part of the examination to rule out acutearct.

A HEAD AND NECKmany institutions, MRA is more often done in the

bacute setting, after the initial stroke work-up is com-te and the tPA window has passed. This is simply

cause MRI is usually not as readily available and hastorically taken longer than CT, although new MRoke protocols performed at certain acute stroke centers

approaching CT in regards to time. Nevertheless, as

th CT, the arteries are assessed for significant stenosis, areclusion, and dissection. Noncontrast (2-dimensionale of flight, 3-dimensional time of flight) or contrast-

hanced MRA techniques can be performed, and whichutilized typically depends on local radiologist prefer-ce. However, contrast-enhanced MRA is thought to bere accurate in imaging extracranial stenosis and vesselrphology than nonenhanced MRA techniques, and

ows general agreement with conventional angiography85%-90% of cases, as does CTA.5 For intracranialnosis, CTA and conventional angiography have beent to be more accurate than MRA.5 Due to advances inRI, contrast-enhanced MRA of the supra-aortic arteriesluding the neck and brain can be obtained with iso-pic submillimeter voxel size with high diagnosticality and excellent intermodality agreement with otherss-sectional techniques such as CTA and time-of-ht MRA.9,10 In addition to depiction of the cervical

sculature, the large, proximal intracranial vessels arell seen, which is of particular use in the acute stroketing. Interventionalists look for thrombus in thesege vessels when considering intra-arterial therapyigure 4C), not in the smaller more distal vessels, which

not as well resolved.

PERFUSIONperfusion has been incorporated into acute stroke im-

ing in many large stroke centers where interventionalatment options such as intra-arterial tPA and clot retrieval

available.11,12 The goal of MR perfusion is to detectrfusion-diffusion mismatch with the implication of sal-geable tissue that can benefit from further therapeutictions. Over the last decade, several clinical trials havegested that patients with a mismatch between their in-

ction volume and the volume of hypoperfused tissue maypond to reperfusion therapies.11-13Commonly used MR perfusion techniques, including ar-ial spin labeling and dynamic susceptibility contrast per-ion, have been long used for evaluation of cerebral per-ion in patients with stroke, each with different strengths

d limitations.14,15 Faster image acquisition and the abilitygenerate perfusion maps in a few minutes have madenamic susceptibility contrast a more robust and widelyepted technique to measure cerebral perfusion in patients

th acute stroke.Although the technique is significantly different, the ba-premise of MR perfusion is similar to CT perfusion:

hemic brain has increased MTT, decreased CBF, andrmal CBV; infarcted brain has increased MTT, decreasedF, and markedly decreased to no CBV. As in CT perfu-n, in MR perfusion it is the presence or absence of bloodthe brain parenchyma (CBV) that allows one to differ-tiate ischemic from infarcted brain. DWI is used to assess

core area of infarct (similar to CBV), while specificrfusion-weighted images (ie, MTT, CBF) represent the

a of ischemia. When there is an abnormal area of perfu-

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385Khan et al Acute Stroke Imagingn that is greater than the area of abnormal diffusionWI), there is an ischemic penumbra.

NVENTIONAL ANGIOGRAPHY (AKA, DIGITALBTRACTION ANGIOGRAPHY)nventional angiography is still considered the gold stan-rd for the detection of cervical and cerebrovascular dis-e and is particularly important when considering inva-e therapies. It also can provide valuable informationout collateral flow, perfusion status, and may detect othercult vascular lesions. The resolution, sensitivity, andcificity of conventional angiography is equal to orater than that of noninvasive techniques.6 Although rel-

vely safe, there is a chance of permanent neurologicalficit, including death, due to the presence of the catheterthe carotid artery. In experienced hands, this is 1%. Inrt because of this and the ready availability and relativee of use of the noninvasive techniques, conventional

giography is typically reserved for cases that may requirera-arterial treatment.

NCLUSIONis article reviewed the many imaging studies available inacute stroke setting. The utility of each study and the

rtinent main findings associated with each were reviewed,was the appropriateness of which study and when eachuld be ordered. A suggested imaging algorithm for acute

oke patients also is presented (Figure 5). The authors

CT without contrast(most instuons)

CTA Head & Neck

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*many radiologists feel more condent excluding blood**for those radiologists who prefer CTA to M

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Figure 5 Suggested acute stroke imaginMRImagnetic resonance imaging; CTApe that our readers have a more clear understanding ofoke imaging that will translate into a tailored imagingrkup.

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MRI without contrastsome instuons with MRI and tech

coverage readily available 24/7)

MRA Head & Neck

MR Perfusion of Head(includes DWI if not already done)

grampeucs)

n CT and will then use the MR paradigmwant to ulize MR Perfusion

chart. CT computed tomography;ngiography; MRAMR angiography.2.

3.

4.

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6.

7.

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enhanced MR angiography at 3.0 Thighly accelerated parallel ac-

quisition for improved spatial resolution over an extended field ofview. Radiology. 2007;242(2):600-609.

10. Villablanca JP, Nael K, Habibi R, Nael A, Laub G, Finn JP. 3 Tcontrast-enhanced magnetic resonance angiography for evaluation ofthe intracranial arteries: comparison with time-of-flight magnetic res-onance angiography and multislice computed tomography angiogra-phy. Invest Radiol. 2006;41(11):799-805.

11. Hacke W, Albers G, Al-Rawi Y, et al. The Desmoteplase in AcuteIschemic Stroke trial (DIAS): a phase II MRI-based 9-hour windowacute stroke thrombolysis trial with intravenous desmoteplase. Stroke.2005;36(1):66-73.

12. Albers GW, Thijs VN, Wechsler L, et al. Magnetic resonance imagingprofiles predict clinical response to early reperfusion: the diffusion and

perfusion imaging evaluation for understanding stroke evolution(DEFUSE) study. Ann Neurol. 2006;60(5):508-17.

13. Davis SM, Donnan GA, Parsons MW, et al. Effects of alteplasebeyond 3 h after stroke in the Echoplanar Imaging ThrombolyticEvaluation Trial (EPITHET): a placebo-controlled randomised trial.Lancet Neurol. 2008;7(4):299-309.

14. Sorensen AG, Buonanno FS, Gonzalez RG, et al. Hyperacute stroke:evaluation with combined multisection diffusion-weighted and hemo-dynamically weighted echo-planar MR imaging. Radiology. 1996;199(2):391-401.

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386 The American Journal of Medicine, Vol 126, No 5, May 2013

Acute Stroke Imaging: What Clinicians Need to KnowNoncontrast Head CTCT Angiography of the Head and NeckCT PerfusionMriMRA Head and NeckMR PerfusionConventional Angiography (aka, Digital Subtraction Angiography)ConclusionReferences