Guidelines
Guidelines Summary
American College of Radiology
The ACR Appropriateness Criteria for Cerebrovascular Disease includes the following key recommendations for stroke imaging [133] :
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Screening for carotid artery stenosis can be performed noninvasively with duplex ultrasound, contrast-enhanced MRA, or CTA.
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Digital Subtraction Angiography (DSA) is the gold standard for carotid artery evaluation and should be performed if noninvasive imaging is inconclusive or contradictory.
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Evaluation of cerebrovascular reserve with CT or MR perfusion with acetazolamide challenge may identify patients at higher risk for stroke due to poor collateral circulation.
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Imaging evaluation of TIA should be performed as soon as possible and is ideally performed with contrast-enhanced brain MRI along with 3-D time-of-flight (TOF) MRA of the circle of Willis and contrast-enhanced MRA of the neck vasculature.
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Noncontrast head CT is the first-line imaging test for acute stroke patients to rule out intracranial hemorrhage and large infarct.
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When possible, CTA should be the next imaging study after intravenous tissue plasminogen activator (IV-tPA) administration in acute stroke patients to evaluate for large-vessel occlusion as a target for intra-arterial therapy
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Patients presenting with acute stroke beyond the 6-hour treatment window are ideally evaluated with contrast-enhanced brain MRI along with 3-D TOF-MRA of the circle of Willis and CE-MRA of the neck vasculature. Age of the infarct can be determined with contrast-enhanced brain MRI.
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Patients with risk factors for cerebral aneurysms can undergo noninvasive screening with TOF-MRA or CTA.
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The initial imaging study in patients presenting with suspected nontraumatic intracranial hemorrhage, whether SAH or intraparenchymal hemorrhage, should be noncontrast head CT.
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Initial evaluation in patients with acute nontraumatic SAH could start with DSA or noninvasive imaging with CTA or MRA. If the initial DSA is negative, then CTA or MRA should subsequently be performed. If CTA or MRA was performed as the initial imaging test and was negative, then DSA should be performed for further evaluation. If both initial DSA and noninvasive studies are negative, DSA should be repeated in 1–2 weeks.
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Unruptured aneurysms that are incidentally discovered on noninvasive imaging should be followed using the same noninvasive imaging modality on which the initial diagnosis was made.
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Definitive diagnosis of cerebral vasospasm after SAH is made with catheter angiography.
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Screening for vasospasm is performed with transcranial Doppler (TCD) ultrasound. CTA or MRA may be useful in the setting of indeterminate TCD ultrasound results.
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Intraparenchymal cerebral hemorrhages that have the classic clinical history and imaging appearance indicative of hypertensive hemorrhage usually do not require further imaging workup other than follow-up noncontrast head CT to evaluate for hemorrhage evolution and complications.
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Intraparenchymal cerebral hemorrhages that do not have the classic clinical history and imaging appearance for hypertensive hemorrhage should undergo further parenchymal and vascular imaging with contrast-enhanced brain MRI, MRA, and sometimes MRV. CT, CTA, and sometimes CTV are imaging alternatives.
Media Gallery
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Axial noncontrast computed tomography (NCCT) demonstrates diffuse hypodensity in the right lentiform nucleus, with mass effect upon the frontal horn of the right lateral ventricle. The patient is a 70-year-old female with history of left-sided weakness for several hours duration.
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MRI was subsequently obtained in the same patient. An axial T2 FLAIR image (left) demonstrates high signal in the lentiform nucleus with mass effect. The axial diffusion-weighted image (middle) demonstrates high signal in the same area with corresponding low signal on the apparent diffusion coefficient (ADC) maps, consistent with true restricted diffusion and an acute infarction. Maximum intensity projection from a 3D time-of-flight MRA (right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
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Axial noncontrast CT scan of the brain in a 60-year-old male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of hemorrhage.
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Noncontrast CT of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial MRI (middle image) demonstrates the hemorrhage with surrounding high-signal edema. The coronal gradient echo image (right) demonstrates susceptibility related to the hematoma with markedly low signal adjacent the left caudate head. Gradient echo images are highly sensitive for blood products.
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Noncontrast CT (left) obtained after this 75-year-old male was admitted for CVA; scan demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. Massive hemorrhagic transformation occurs by day 6 (right) with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted, layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.
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This 60-year-old female underwent NCCT after an episode of left upper extremity weakness. NCCT demonstrates cortical and subcortical hypodensity involving the right mid to anterior temporal lobe.
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MIP image from a CTA demonstrates a filling defect or high-grade stenosis at the branching point of the right MCA trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large vessel stenosis and occlusions, which comprise approximately one third of ischemic strokes.
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Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon.
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Axial noncontrast CT demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in this 60-year-old male with new onset of right-sided weakness. The lesion demonstrates high signal on the FLAIR sequence (middle image) and DWI (right image), with low signal on the ADC maps, indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem, and cerebellum.
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Noncontrast CT scan was performed emergently in this 71-year-old male who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. Diffuse loss of gray-white differentiation is present. The FLAIR image demonstrates high signal throughout the cortical sulci, basilar cisterns, and in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage because of the suppression of high CSF signal lending to greater conspicuity of SAH compared with conventional MRI sequences.
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MRI was obtained to evaluate this 62-year-old hypertensive and diabetic male with history of transient episodes of right-sided weakness and aphasia. The FLAIR image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep borderzone or watershed infarction; in this case, the anterior and posterior middle cerebral artery (MCA) watershed areas. The left-sided infarcts have corresponding low signal on the ADC map (right), signifying acuity. An old left posterior parietal infarct is noted as well.
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This patient subsequently underwent a CTA and subsequent cerebral angiography. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery (ICA) injection. Balloon-assisted coil embolization was performed.
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Middle cerebral artery (MCA) occlusion: This patient was a 64-year-old male who presented within 3 hours of onset of aphasia and right-sided weakness. Frontal view from a selective injection of the left internal carotid artery during a cerebral angiogram demonstrates filling of the anterior cerebral artery with an abrupt cut-off at the middle third of the M1 segment of the left MCA with no distal filling.
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Noncontrast CT was obtained to evaluate this 64-year-old male who awoke with aphasia and right-sided weakness. Loss of the normal gray-white differentiation between the normally denser insular cortex and the less attenuating subinsular white matter is seen; this is consistent with loss of the "insular ribbon."
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Follow-up noncontrast CT scan obtained approximately 12 hours after the initial study in the same patient demonstrates further evolution of the infarction, which is now extensive and spans most of the left middle cerebral artery (MCA) territory.
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Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.
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Noncontrast CT scanning was performed to evaluate this 70-year-old female with a history of acute onset of right-hand weakness and aphasia. Loss of gray-white differentiation in the left insular cortex and in the immediately adjacent cortical and subcortical portions of the left temporal operculum is seen; this is strongly suggestive of an acute infarction.
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Noncontrast CT scan from the patient in the previous image is re-examined using narrower windows to accentuate any hypodensity (window width, 10 HU; center, 30 HU). The hypodensity in the insular and subinsular regions is more conspicuous. Using varying window width and center levels can aid in the detection of early ischemic changes.
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Noncontrast CT scan in an 80-year-old female who presented with acute onset of right-sided weakness. The left middle cerebral artery (MCA) trunk appears highly attenuated (the dense MCA sign), suspicious for acute thrombosis or embolism. A follow-up noncontrast CT demonstrated an evolving infarct of the lentiform nucleus.
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Dense middle cerebral artery (MCA) sign: Noncontrast CT in another patient with strokelike symptoms demonstrates a hyperdense appearance of the right MCA with subtle loss of gray-white differentiation of the anterior right temporal lobe.
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A follow-up noncontrast CT scan of the brain; this was obtained in the patient in the previous image and demonstrates diffuse hypodensity with loss of gray-white differentiation and sulcal effacement in most of the right middle cerebral artery (MCA) territory, with mass effect upon the left lateral ventricle and leftward midline shift consistent with an acute infarction.
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Dense basilar artery: Axial noncontrast CT scan demonstrates a hyperdense basilar artery in a patient with pontine infarction who was later found to have basilar artery thrombosis. Other large vessels besides the middle cerebral artery (MCA) can produce a dense vessel sign when occluded.
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Chronic infarction: Noncontrast CT scan demonstrates a well-defined area of volume loss in the right temporal lobe with a low-density appearance consistent with encephalomalacia. No mass effect exists.
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Thrombolytic therapy carries a small but significant risk of life-threatening hemorrhage. For this reason, carefully screening for exclusionary criteria prior to administering tPA is important; this criteria includes hemorrhage, large areas of infarction, and patient presentation beyond the 3-hour window for IV tPA or possibly beyond 6 hours for IA tPA. This case illustrates this point in a patient with normal NCCT who was treated with IV tPA for acute stroke and, over the next 2 days, developed significant hemorrhage. Hemorrhage is noted to progressively increase in size along the medial margin of the right thalamus and the third ventricle. Obstructive hydrocephalus with hemorrhage layering is seen in the dependent portions of the occipital horns.
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MIP and surface volume rendered images of the circle of Willis from a CTA in a 70-year-old female with acute onset right-sided weakness. A high-grade stenosis of the distal left middle cerebral artery (MCA) trunk (red circles) is seen, with filling of the remainder of the MCA territory via an anterior branch near the bifurcation.
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CTA source data can also be useful to assess for areas of hypoperfusion and poor enhancement that may correspond to areas of greatest ischemia. This CTA source image from the patient in the previous case demonstrates significantly diminished enhancement involving the caudate head, lentiform nucleus, and capsular regions. High density noted centrally in this poorly enhancing region represents an area of hemorrhagic transformation.
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Placement of ROI curves on arterial and venous pixels (image on right) are needed to generate time-concentration curves for perfusion imaging. These curves can then be used to generate perfusion maps.
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After selecting the appropriate arterial and venous input functions, the computer software is able to generate perfusion maps of different parameters (CBF = cerebral blood flow, CBV = cerebral blood Volume, MTT = mean transit time, TTP = time to peak enhancement). Regions of interest can then be placed over these maps for quantitative information. In this patient with occlusion of the distal left MCA trunk, elevated MTT and diminished CBF exists in the left basal ganglia, insular and opercular regions. The CBV is mildly increased in this same region, which is believed to be due to autoregulatory vasodilation in response to ischemia.
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Axial FLAIR image demonstrates intra-arterial high signal in the left middle cerebral artery (MCA) of this patient with early stroke. The intra-arterial high signal has been postulated to be secondary to different factors, including stasis, slow or reversed flow, and thrombus.
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Noncontrast CT scan and MRI of the brain with DWI was performed to evaluate this 87-year-old male with history of recurrent strokes and new change in mental status. Noncontrast CT scan demonstrates a right PCA distribution hypodensity, and a hypodensity at the vertex on the right near the MCA/ACA borderzone. Both of these abnormalities are age indeterminate on the CT scan.
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MRI was obtained to further clarify the findings on a noncontrast CT scan. High signal on the DWI and corresponding low signal on the ADC maps in the right frontal vertex borderzone area are seen. This signifies true restricted diffusion and an acute infarction.
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The right posterior cerebral artery (PCA) distribution infarction is most likely chronic. The high signal on the DWI has no corresponding low signal on the ADC map (red circle). The ADC map demonstrates slightly elevated signal in this case. The falsely persistent high signal on DWI in the absence of recent infarction is felt to be related to the partial T2-effects of DWI and is referred to as "T2 shine through."
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Axial T1-weighted postcontrast image obtained in a patient with recent stroke demonstrates arterial enhancement within the left middle cerebral artery (MCA) as well as cortical and subcortical enhancement in the adjacent insular and opercular regions. The arterial enhancement is believed to be due to slow flow and underlying impaired hemodynamics. Early parenchymal enhancement may indicate good collateral supply.
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TOF MRA demonstrates an occlusion or high-grade stenosis at the mid to distal right middle cerebral artery (MCA) trunk. MRA is highly accurate at helping to evaluate large intracerebral vessel stenosis, although less reliable than CT scanning at helping to grade stenosis.
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3D time-of-flight (TOF) of the neck axial and MIP images demonstrates a 2-cm low-signal curvilinear dissection flap in the mid right vertebral artery. This patient has a history of fibromuscular dysplasia and prior carotid artery dissection.
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Left internal carotid artery (ICA) occlusion: Axial FLAIR images demonstrate high signal in the centrum semiovale in the deep borderzone region with corresponding restricted diffusion, indicating infarction. MIP from a time-of-flight MRA of the circle of Willis demonstrates no flow in the left ICA or anterior circulation on the right.
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Left internal carotid artery (ICA) occlusion: MR perfusion imaging demonstrates global and marked elevation in mean transit time (image on left) in most of the left cerebral hemisphere, sparing only part of the posterior circulation. This demonstrates how MTT is extremely sensitive to abnormalities in perfusion. The CBV (image on right) is markedly depressed more centrally in the deep and subcortical white matter, consistent with the infarction noted on DWI.
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Color Doppler ultrasound of the left internal carotid artery was obtained in a 57-year-old male with history of transient ischemic attacks. A large amount of plaque is seen in the proximal left internal carotid artery producing a high-grade stenosis. However, color flow is noted distal to the stenosis.
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Pulsed Doppler waveforms in the same patient demonstrate a markedly elevated peak systolic velocity in the proximal internal carotid artery (ICA) of 252 cm/s. The second waveform, obtained more distally in the same stenosis, demonstrates a velocity of greater than 400 cm/s. The stenosis is more than 70 and, based on gray scale and color flow assessment, appears near occlusive. This illustrates the importance of carefully sampling along the course of a stenosis for the highest peak systolic velocity.
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Digital subtraction angiogram performed in the same patient as previous photo confirms the near occlusion with a "string sign" in the proximal left internal carotid artery.
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Transcranial Doppler demonstrates pulsatile flow in the right-middle cerebral artery in a 40-year-old patient following subarachnoid hemorrhage and vasospasm. At a depth of 58 mm (near the origin of the middle cerebral artery [MCA]), a markedly elevated peak systolic flow velocity of approximately 251 cm/s and a mean velocity of approximately 164 cm/s indicates severe MCA stenosis. Normal peak and mean MCA flow velocities are approximately 100 cm/s and 50 cm/s, respectively.
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Noncontrast CT of the brain in a patient with history of remote CVA demonstrates low density in the right frontal and anterior temporal regions in the MCA distribution. Evidence of parenchymal volume loss with ex-vacuo dilatation of the right lateral ventricle is present, indicating chronicity infarction.
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Noncontrast CT in this 52-year-old male with history of worsening right-sided weakness and apahasia demonstrates diffuse hypodensity and sulcal effacement involving the left anterior and middle cerebral artery territories consistent with acute infarction. Scattered curvilinear areas of hyperdensity are suggestive of developing petechial hemorrhage in this large area of infarction.
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MRA in the same patient (left) demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal middle cerebral artery (MCA) trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the ADC map consistent with acute infarction.
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Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the the origin of the callosomarginal branch of the anterior cerebral artery (ACA). The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery (MCA), with the apex representing the Sylvian point.
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Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SICA) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries.
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Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The MCA can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches) and M4 (distal cortical branches on the lateral hemispheric convexities).
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Frontal view from a cerebral angiogram in a 41-year-old male who presented 7 days prior with subarachnoid hemorrhage from a ruptured anterior communicating artery aneurysm treated with surgical clipping. Significant narrowing of the proximal left anterior cerebral artery (ACA), left M1 segment, and left supraclinoid internal carotid artery (ICA) indicates vasospasm.
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Angiographic view in the same patient (image on left) with superimposed road map image demonstrate placement of a wire across the left M1 segment and balloon angioplasty. The left proximal anterior cerebral artery (ACA) and supraclinoid internal carotid artery (ICA) were also angioplastied and intra-arterial verapamil was administered. Follow-up image on the right after treatment demonstrates resolution of the left M1 segment and distal ICA, which are now widely patent. Residual narrowing is seen in the left proximal ACA.
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Regions of interest are selected for arterial and venous input (image on left) for dynamic susceptibility-weighted perfusion MRI. Signal-time curves (image on right) obtained from these ROI demonstrate transient signal drop following the administration of intravenous contrast. The information obtained from the dynamic parenchymal signal changes post contrast are used to generate maps of different perfusion parameters.
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Vascular distributions: Middle cerebral artery (MCA) infarction. Noncontrast CT scan demonstrates a large acute infarction in the MCA territory involving the lateral surfaces of the left frontal, parietal, and temporal lobes as well as the left insular and subinsular regions with mass effect and rightward midline shift. The caudate head is spared, and at least part of the lentiform nucleus and internal capsule, which receive blood supply form the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (anterior cerebral artery territory), thalami and paramedian occipital lobe (posterior cerebral artery territory).
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Vascular distributions: Anterior choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with associated signal dropout on the apparent diffusion coefficient (ADC) map involving the posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal artery, the last branch of the internal carotid artery before bifurcating into the anterior and middle cerebral arteries. The anterior choroidal artery may also arise from the middle cerebral artery (MCA).
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Vascular distributions: anterior cerebral artery (ACA) infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. Infarction of the lateral temporoparietal regions bilaterally (both MCA distributions) also exists; it is greater on the left, indicating multivessel involvement suggesting emboli.
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Vascular distributions: posterior cerebral artery (PCA) infarction. The noncontrast CT images demonstrate PCA distribution infarction involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional involvement of the thalamus, also part of the PCA territory.
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Cerebral angiogram was performed in a 57-year-old male with family history of subarachnoid hemorrhage and found on previous imaging to have a left distal internal carotid artery (ICA) aneurysm. The lateral projection from the angiogram demonstrates a narrow-necked aneurysm arising off the posterior aspect of the distal supraclinoid left ICA with an additional nipple-like projecting off the inferior aspect of the dome of the aneurysm. Mild lobulated dilatation of the cavernous left ICA is also present.
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Follow-up cerebral angiogram in the same patient as previous image after coil embolization. Multiple coils were placed with sequential occlusion of the aneurysm, including the nipple at its inferior aspect. A small amount of residual filling is noted at the proximal neck of the aneurysm, which may thrombose over time.
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The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (MCA; red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal and anterior temporal lobes, insula, and basal ganglia. The anterior cerebral artery (ACA; blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (PCA; green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
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CT fogging effect: Axial noncontrast CT scan demonstrates focal low density, loss of gray-white differentiation, and mild sulcal effacement in the right parietal region (left image, arrow) in a 62-year-old female presenting with acute stroke. A follow-up noncontrast CT scan obtained 10 days later demonstrates diminished sulcal effacement and isodensity with a near-normal appearance (middle image), thought to be secondary to the CT "fogging effect" that may be seen during the evolution of an infarct. The axial diffusion-weighted image (right) confirms the right parietal infarct.
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ASPECTS quantitative stroke scoring system: For ASPECTS scoring, the middle cerebral artery (MCA) territory is allotted 1 point for each of 10 separate regions: M1, M2, M3, M4, M5, M6, the caudate nucleus (C), lentiform nucleus (L), insular cortex (I), and internal capsule (IC). Scoring is based on a section at the level of the basal ganglia and thalami and another section above the level at the basal ganglia. One point is subtracted for each area demonstrating signs of early ischemic change, such as focal parenchymal hypoattenuation or edema. A normal scan would be scored a 10, and diffuse edema involving all points would be scored 0.
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Noncontrast CT scan performed in a 60-year-old male who presented with acute stroke demonstrates the use of the ASPECTS. Diffuse hypodensity is noted throughout the middle cerebral artery (MCA) distribution involving the M1-M6 regions and insula. Seven points are then subtracting from the 10-point ASPECTS, yielding a score of 3. C = caudate nucleus, L = lentiform nucleus, I = insular cortex, and IC = internal capsule.
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