Approach Considerations
Imaging studies
Emergent brain imaging is essential for excluding mimics (SAH, ICH, masses) and potentially confirming the diagnosis of ischemic stroke. Noncontrast CT scanning is the most commonly used form of neuroimaging in the acute evaluation of patients with apparent acute stroke. A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT scan is negative but the clinical suspicion remains high. Multimodal CT imaging with the addition of CT angiography and CT perfusion to NCCT has the potential to identify large vessel occlusions and areas of salvagable tissue.
MRI with magnetic resonance angiography (MRA) has been a major advance in the neuroimaging of stroke. MRI not only provides great structural detail but also can demonstrate early cerebral edema. In addition, MRI has proved to be sensitive for detection of acute intracranial hemorrhage. However, MRI is not as available as CT scanning is in emergencies, many patients have contraindications to MRI imaging (eg, pacemakers, implants), and interpretation of MRI scans may be more difficult.
Carotid duplex scanning is one of the most useful tests in evaluating patients with stroke. Increasingly, it is being performed earlier in the evaluation, not only to define the cause of the stroke but also to stratify patients for either medical management or carotid intervention if they have carotid stenoses.
Digital subtraction angiography is considered the definitive method for demonstrating vascular lesions, including occlusions, stenoses, dissections, and aneurysms.
For more information, see Cerebral Revascularization Imaging.
Laboratory studies
Extensive laboratory testing is not routinely required before decisions are made regarding fibrinolysis. Testing can often be limited to blood glucose, plus coagulation studies if the patient is on warfarin, heparin, or one of the newer antithrombotic agents (eg, dabigatran, rivaroxaban). A complete blood count (CBC) and basic chemistry panel can be useful baseline studies.
Additional laboratory tests are tailored to the individual patient and may include the following:
-
Cardiac biomarkers
-
Toxicology screen
-
Fasting lipid profile
-
Erythrocyte sedimentation rate
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Pregnancy test
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Antinuclear antibody (ANA)
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Rheumatoid factor
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Homocysteine level
-
Rapid plasma reagent (RPR)
A urine pregnancy test should be obtained for all women of childbearing age with stroke symptoms. The safety of the fibrinolytic agent recombinant tissue-type plasminogen activator (rt-PA) in pregnancy has not been studied in humans (ie, the agent is in the FDA pregnancy category C).
Brain Imaging With CT Scanning and MRI
CT scanning
Imaging with CT scanning has multiple logistic advantages for patients with acute stroke. Image acquisition is faster with CT scanning than with MRI, allowing for assessment with an examination that includes noncontrast CT scanning, CT angiography (CTA), and CT perfusion scanning in a short amount of time. Expedient acquisition is of the utmost importance in acute stroke imaging because of the narrow window of time available for definitive ischemic stroke treatment with pharmacologic agents and mechanical devices.
CT scanning can also be performed in patients who are unable to tolerate an MR examination or who have contraindications to MRI, including implantable pacemakers, some aneurysm clips, or other ferromagnetic materials in their bodies. Additionally, CT scanning is more easily accessible and commonly located in the ED, which is helpful for patients who require special equipment for monitoring or life support. [66, 67]
MRI
Previously, conventional (spin echo) MRI may take hours to produce discernible findings in acute ischemic stroke. Diffusion-weighted imaging (DWI) is highly sensitive to early cellular edema, which correlates well with the presence of cerebral ischemia. For this reason, many centers include DWI in their standard brain MRI protocol. DWI MRI can detect ischemia much earlier than standard CT scanning or spin echo MRI can and provides useful data in patients with stroke or transient ischemic attack (TIA). (See the image below.) [2, 68, 69, 70]
Magnetic resonance imaging (MRI) scan in a 70-year-old woman with a history of left-sided weakness for several hours. An axial T2 fluid-attenuated inversion recovery (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 3-dimensional (3-D) time-of-flight magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
The most commonly used technique for perfusion MRI is dynamic susceptibility, which involves generating maps of brain perfusion by monitoring the first pass of a rapid bolus injection of contrast through the cerebral vasculature. Susceptibility-related T2 effects create signal loss in capillary blood vessels and parenchyma perfused by contrast.
For more information on MRI and MRA in this setting, see Magnetic Resonance Imaging in Acute Stroke.
Based on the central volume principle, dynamic brain perfusion data can be obtained. Cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time (MTT) can be calculated using either perfusion MRI or CT scanning. (See the image below.)
Regions of interest are selected for arterial and venous input (image on left) for dynamic susceptibility-weighted perfusion magnetic resonance imaging (MRI). Signal-time curves (image on right) obtained from these regions of interest demonstrate transient signal drop following the administration of intravenous contrast. The information obtained from the dynamic parenchymal signal changes postcontrast is used to generate maps of different perfusion parameters.
An evidence-based guideline from the American Academy of Neurology advises that DWI is more useful than noncontrast CT scanning for the diagnosis of acute ischemic stroke within 12 hours of symptom onset and should be performed for the most accurate diagnosis of acute ischemic stroke (level A). No recommendations were made regarding the use of perfusion-weighted imaging (PWI) in diagnosing acute ischemic stroke, as evidence to support or refute its value in this setting is insufficient. [71]
Intra-arterial contrast enhancement may be seen secondary to slow flow during the first or second day after onset of infarction. This finding has been correlated with increased infarct volume size. [72]
Other Imaging Studies in Ischemic Stroke
Transcranial Doppler ultrasonography is useful for evaluating more proximal vascular anatomy—including the middle cerebral artery (MCA), intracranial carotid artery, and vertebrobasilar artery—through the infratemporal fossa. [73] Echocardiography is obtained in all patients with acute ischemic stroke in whom cardiogenic embolism is suspected.
Chest radiography has potential utility for patients with acute stroke. However, obtaining a chest radiograph should not delay the administration of rt-PA, as radiographs have not been shown to alter the clinical course or decision-making in most cases. [74]
The use of single-photon emission CT (SPECT) scanning in stroke is still experimental and is available only at select institutions. Theoretically, it can define areas of altered regional blood flow. [75]
Conventional angiography is the gold standard in evaluating for cerebrovascular disease as well as for disease involving the aortic arch and great vessels in the neck. Conventional angiography can be performed to clarify equivocal findings or to confirm and treat disease seen on MRA, CTA, transcranial Doppler, or ultrasonography of the neck. (See the images below.)
A 48-year-old man presented with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference. Angiogram with selective injection of the right internal carotid artery demonstrates occlusion of the M1 segment of the right middle cerebral artery (MCA) and A2 segment of the right anterior cerebral artery (ACA; images courtesy of Concentric Medical).
Follow-up imaging after mechanical embolectomy in 48-year-old man with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference demonstrates complete recanalization of the right middle cerebral artery (MCA) and partial recanalization of the right A2 segment (images courtesy of Concentric Medical).
Cerebral angiogram performed approximately 4.5 hours after symptom onset in a 31-year-old man demonstrates an occlusion of the distal basilar artery (images courtesy of Concentric Medical).
Image on the left demonstrates deployment of a clot retrieval device (older generation device) in a 31-year-old man. Followup angiogram after embolectomy demonstrates recanalization of the distal basilar artery with filling of the superior cerebellar arteries and posterior cerebral arteries. The patient had complete resolution of symptoms following embolectomy (images courtesy of Concentric Medical).
Blood Studies
A CBC serves as a baseline study and may reveal a cause for the stroke (eg, polycythemia, thrombocytosis, thrombocytopenia, leukemia), identify evidence of concurrent illness (eg, anemia), or issues that may affect reperfusion strategies (thrombocytopenia). The basic chemistry panel serves as a baseline study and may reveal a stroke mimic (eg, hypoglycemia, hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency).
Coagulation studies may reveal a coagulopathy and are useful when fibrinolytics or anticoagulants are to be used. In patients who are not taking anticoagulants or antithrombotics and in whom there is no suspicion for coagulation abnormality, administration of rt-PA should not be delayed while awaiting laboratory results.
Cardiac biomarkers are important because of the association of cerebral vascular disease and coronary artery disease. Additionally, several studies have indicated a link between elevations of cardiac enzyme levels and poor outcome in ischemic stroke.
Toxicology screening may be useful in selected patients in order to assist in identifying intoxicated patients with symptoms/behavior mimicking stroke syndromes or to identify sympathomemetic (cocaine) use, which may be the cause of the ischemic or hemorrhagic stroke . In patients with suspected hypoxemia, arterial blood gas studies define the severity of hypoxemia and may detect acid-base disturbances. However, arterial punctures should be avoided unless absolutely necessary in patients being considered for fibrinolytic therapy.
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Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.
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Axial noncontrast computed tomography (NCCT) scan demonstrates diffuse hypodensity in the right lentiform nucleus with mass effect upon the frontal horn of the right lateral ventricle in a 70-year-old woman with a history of left-sided weakness for several hours.
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Magnetic resonance imaging (MRI) scan in a 70-year-old woman with a history of left-sided weakness for several hours. An axial T2 fluid-attenuated inversion recovery (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 3-dimensional (3-D) time-of-flight magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
-
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 computed tomography (CT) scan demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in a 60-year-old man with acute onset of right-sided weakness. The lesion demonstrates high signal on the fluid-attenuated inversion recovery (FLAIR) sequence (middle image) and diffusion-weighted magnetic resonance imaging (MRI) scan (right image), with low signal on the apparent diffusion coefficient (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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Magnetic resonance imaging (MRI) scan was obtained in a 62-year-old man with hypertension and diabetes and a history of transient episodes of right-sided weakness and aphasia. The fluid-attenuated inversion recovery (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 border-zone, 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 apparent diffusion coefficient (ADC) map (right), signifying acuity. An old left posterior parietal infarct is noted as well.
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A 48-year-old man presented with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference. Angiogram with selective injection of the right internal carotid artery demonstrates occlusion of the M1 segment of the right middle cerebral artery (MCA) and A2 segment of the right anterior cerebral artery (ACA; images courtesy of Concentric Medical).
-
Follow-up imaging after mechanical embolectomy in 48-year-old man with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference demonstrates complete recanalization of the right middle cerebral artery (MCA) and partial recanalization of the right A2 segment (images courtesy of Concentric Medical).
-
Cerebral angiogram performed approximately 4.5 hours after symptom onset in a 31-year-old man demonstrates an occlusion of the distal basilar artery (images courtesy of Concentric Medical).
-
Image on the left demonstrates deployment of a clot retrieval device (older generation device) in a 31-year-old man. Followup angiogram after embolectomy demonstrates recanalization of the distal basilar artery with filling of the superior cerebellar arteries and posterior cerebral arteries. The patient had complete resolution of symptoms following embolectomy (images courtesy of Concentric Medical).
-
Noncontrast computed tomography (CT) scan in a 52-year-old man with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement with mass effect involving the left anterior and middle cerebral artery territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity noted suggestive of developing petechial hemorrhage in this large area of infarction.
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Magnetic resonance angiogram (MRA) in a 52-year-old man 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 apparent diffusion coefficient (ADC) map consistent with acute infarction.
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Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the 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 (PICAs) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICAs) arise from the proximal basilar artery. The superior cerebellar arteries (SCAs) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries (PCAs).
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Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery (ICA) illustrates the anterior circulation. The anterior cerebral artery (ACA) consists of the A1 segment proximal to the anterior communicating artery, with the A2 segment distal to it. The middle cerebral artery (MCA) can be divided into 4 segments: the M1 (horizontal segment) extends to the anterior basal portion of the insular cortex (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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Regions of interest are selected for arterial and venous input (image on left) for dynamic susceptibility-weighted perfusion magnetic resonance imaging (MRI). Signal-time curves (image on right) obtained from these regions of interest demonstrate transient signal drop following the administration of intravenous contrast. The information obtained from the dynamic parenchymal signal changes postcontrast is used to generate maps of different perfusion parameters.
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Vascular distributions: Middle cerebral artery (MCA) infarction. Noncontrast computed tomography (CT) scanning 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. There is sparing of the caudate head and at least part of the lentiform nucleus and internal capsule, which receive blood supply from the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (anterior cerebral artery [ACA] territory), thalami, and paramedian occipital lobe (posterior cerebral artery [PCA] 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 (ICA) 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. There is also infarction of the lateral temporoparietal regions bilaterally (both middle cerebral artery [MCA] distributions), greater on the left indicating multivessel involvement and suggesting emboli.
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Vascular distributions: Posterior cerebral artery (PCA) infarction. The noncontrast computed tomography (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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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.
Tables
VASCULAR TERRITORY |
Structures Supplied |
Anterior Circulation (Carotid) |
|
Anterior Cerebral Artery |
Cortical branches: medial frontal and parietal lobe Medial lenticulostriate branches: caudate head, globus pallidus, anterior limb of internal capsule |
Middle Cerebral Artery |
Cortical branches: lateral frontal and parietal lobes, lateral and anterior temporal lobe Lateral lenticulostriate branches: globus pallidus and putamen, internal capsule |
Anterior Choroidal Artery |
Optic tracts, medial temporal lobe, ventrolateral thalamus, corona radiata, posterior limb of the internal capsule |
Posterior Circulation (Vertebrobasilar) |
|
Posterior Cerebral Artery |
Cortical branches: occipital lobes, medial and posterior temporal and parietal lobes Perforating branches: brainstem, posterior thalamus and midbrain |
Posterior Inferior Cerebellar Artery |
Inferior vermis; posterior and inferior cerebellar hemispheres |
Anterior Inferior Cerebellar Artery |
Anterolateral cerebellum |
Superior Cerebellar Artery |
Superior vermis; superior cerebellum |
|
Category |
Description |
Score |
1a |
level of consciousness (LOC) |
Alert Drowsy Stuporous Coma |
0 1 2 3 |
1b |
LOC questions (month, age) |
Answers both correctly Answers 1 correctly Incorrect on both |
0 1 2 |
1c |
LOC commands (open and close eyes, grip and release nonparetic hand) |
Obeys both correctly Obeys 1 correctly Incorrect on both |
0 1 2 |
2 |
Best gaze (follow finger) |
Normal Partial gaze palsy Forced deviation |
0 1 2 |
3 |
Best visual (visual fields) |
No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia |
0 1 2 3 |
4 |
Facial palsy (show teeth, raise brows, squeeze eyes shut) |
Normal Minor Partial Complete |
0 1 2 3 |
5 |
Motor arm left* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
6 |
Motor arm right* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
7 |
Motor leg left* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
8 |
Motor leg right* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
9 |
Limb ataxia (finger-nose, heel-shin) |
Absent Present in 1 limb Present in 2 limbs |
0 1 2 |
10 |
Sensory (pinprick to face, arm, leg) |
Normal Partial loss Severe loss |
0 1 2 |
11 |
Extinction/neglect (double simultaneous testing) |
No neglect Partial neglect Complete neglect |
0 1 2 |
12 |
Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty") |
Normal articulation Mild to moderate dysarthria Near to unintelligible or worse |
0 1 2 |
13 |
Best language** (name items, describe pictures) |
No aphasia Mild to moderate aphasia Severe aphasia Mute |
0 1 2 3 |
|
Total |
- |
0-42 |
* For limbs with amputation, joint fusion, etc, score 9 and explain ** For intubation or other physical barriers to speech, score 9 and explain. Do not add 9 to the total score. NIH Stroke Scale (PDF) |
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