Ischemic Stroke in Emergency Medicine Workup

  • Author: Salvador Cruz-Flores, MD, MPH; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Oct 19, 2011
 

Approach Considerations

Laboratory evaluation of the patient with ischemic stroke should be driven by comorbid illnesses as well as the potential acute stroke. Additional laboratory tests are tailored to the individual patient. They may include rapid plasma reagent (RPR), toxicology screen, fasting lipid profile, sedimentation rate, pregnancy test, antinuclear antibody (ANA), rheumatoid factor, and homocysteine.

CT is the most commonly used form of neuroimaging in the acute evaluation of patients with apparent acute stroke. 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 impaired metabolism.

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.

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Complete Blood Cell Count

CBC count serves as a baseline study and may reveal a cause for the stroke (eg, polycythemia, thrombocytosis, thrombocytopenia, leukemia) or provide evidence of concurrent illness (eg, anemia).

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Basic Chemistry Panel

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).

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Coagulation Studies

Coagulation studies may reveal a coagulopathy and are useful when thrombolytics or anticoagulants are to be used. In patients who are not anticoagulated and in whom there is no suspicion for coagulation abnormality, administration of recombinant tissue-type plasminogen activator (rt-PA) should not be delayed awaiting laboratory studies.

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Cardiac Biomarkers

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.

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Toxicology Screening

Toxicology screening may be useful in selected patients in order to assist in identifying intoxicated patients with symptoms/behavior mimicking stroke syndromes. Urine pregnancy test should be obtained for all women of childbearing age with stroke symptoms. The agent rt-PA is Pregnancy Class C.

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Arterial Blood Gas Analysis

Although infrequent in patients with suspected hypoxemia, arterial blood gas defines the severity of hypoxemia and may detect acid-base disturbances. If considering thrombolytics, arterial punctures should be avoided unless absolutely necessary.

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Imaging in Stroke

Imaging in ischemic stroke can involve several types of MRI, several types of CT scanning, angiography, ultrasonography, radiology, echocardiography, and nuclear imaging studies.

Magnetic resonance imaging

Conventional MRI may take hours to produce discernable findings, well after the diffusion-weighted images have become positive. For this reason, many centers always include diffusion-weighted images in their standard brain MRI protocol. Diffusion-weighted MRI can detect ischemia much earlier than can standard CT scanning or MRI and provides useful data in stroke and TIA patients outside of the initial management window.[18, 41, 42] 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 that can be measured and is proportional to the CBV. (See the image below.)

Regions of interest are selected for arterial and 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 IV 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 recommends that diffusion-weighted imaging (DWI) is more useful than noncontrast CT 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.[43]

Intra-arterial contrast enhancement may be seen secondary to slow flow during the first or second day after onset of infarction and has been correlated with increased infarct volume size.[44]

The 3 different techniques used to produce MRA images are 3-dimensional time of flight (3D TOF), phase-contrast (PC), and contrast-enhanced MRA (CEMRA). Three-dimensional TOF takes advantage of the higher signal from protons in flowing blood, compared with protons in stationary tissue, which become partially saturated and lose signal when exposed to a radiofrequency (RF) pulse. Areas of signal loss and narrowing correspond to stenosis and occlusions. PC involves tagging the spins of moving protons using bidirectional gradients and marking their changes in position when each gradient is applied. PC is exquisitely sensitive to flow, which the operator can choose the velocity threshold for, and gives excellent background suppression. CEMRA utilizes the intraluminal signal produced by a timed bolus of paramagnetic contrast material to evaluate vessel patency. Images may be single phase (i.e. arterial) or time resolved.

For more information, see Magnetic Resonance Imaging in Acute Stroke.

CT scanning

Imaging with computed tomography (CT) scanning has multiple logistic advantages for patients with acute stroke. CT scanning is able to more rapidly acquire images than MRI, allowing for assessment with an examination that includes noncontrast CT scanning, CT angiography, CT perfusion scanning in less than 10 minutes. 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 pacemakers, aneurysm clips, or other ferromagnetic materials in their bodies. Additionally, CT scanning is more easily accessible for patients who require special equipment for maintaining and monitoring life support.[45, 46]

The 2011 AHA/ASA CVT statement notes that MRI is more sensitive for the detection of CVT than CT. However, these modalities do not always accurately reveals positive findings of intraluminal thrombus, which is key to the diagnosis of CVT. Therefore, although a plain CT or MRI is useful in the initial evaluation, a negative finding should not rule out CVT.[40]

Other imaging studies in ischemic stroke

Transcranial Doppler ultrasonography is useful for evaluating more proximal vascular anatomy through the infratemporal fossa, including the MCA, intracranial carotid artery, and vertebrobasilar artery.[47]

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 recombinant tissue-type plasminogen activator (rt-PA); these radiographs have not been shown to alter the clinical course or decision-making in most cases.[48]

The use of SPECT scanning in stroke is still relatively experimental and available only at select institutions; it can theoretically define areas of altered regional blood flow.

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; it also provides for less invasive endovascular interventions. 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.

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Lumbar Puncture

A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT scan is negative but the clinical suspicion remains high.

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Contributor Information and Disclosures
Author

Salvador Cruz-Flores, MD, MPH  Professor of Neurology, Director of Souers Stroke Institute, Department of Neurology and Psychiatry, St Louis University School of Medicine; Director, Mid-America Stroke Network and Neuroscience Critical Care Unit, St Louis University Hospital

Salvador Cruz-Flores, MD, MPH is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Neurology, American College of Physicians, American Heart Association, American Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, and Society of Critical Care Medicine

Disclosure: Axio inc Honoraria Review panel membership; Roche Honoraria Review panel membership; Lilly Honoraria Review panel membership

Coauthor(s)

Jeffrey L Arnold, MD, FACEP  Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose.

Joseph U Becker, MD  Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Everett C Hills, MD, MS  Vice Chair, Department of Physical Medicine and Rehabilitation, Medical Director for Outpatient Services, Penn State Hershey Rehabilitation Hospital; Assistant Professor of Physical Medicine and Rehabilitation, Assistant Professor of Orthopaedics and Rehabilitation, Penn State Milton S Hershey Medical Center and Pennsylvania State University College of Medicine

Everett C Hills, MD, MS is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Congress of Rehabilitation Medicine, American Medical Association, American Society of Neurorehabilitation, Association of Academic Physiatrists, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Edward C Jauch, MD, MS, FAHA, FACEP  Professor, Division of Emergency Medicine and Department of Neurosciences, Medical University of South Carolina

Edward C Jauch, MD, MS, FAHA, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, American Medical Association, National Stroke Association, Society for Academic Emergency Medicine, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Thomas A Kent, MD  Professor and Director of Stroke Research and Education, Department of Neurology, Baylor College of Medicine; Chief of Neurology, Michael E DeBakey Veterans Affairs Medical Center

Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Howard S Kirshner, MD  Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Brett Kissela, MD  MS, Professor, Co-Director of the Neurology Residency Program, Vice-Chair of Education and Clinical Services, Department of Neurology, University of Cincinnati

Brett Kissela, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, and Phi Beta Kappa

Disclosure: Allergan Consulting fee Consulting; Allergan Honoraria Speaking and teaching

Consuelo T Lorenzo, MD  Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health Immanuel Rehabilitation Center

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Richard Salcido, MD  Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Brian Silver, MD, FRCPC, FAHA  Director, Stroke Center, Rhode Island Hospital; Associate Professor of Neurology, The Warren Alpert Medical School of Brown University

Brian Silver, MD, FRCPC, FAHA is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, American Stroke Association, Massachusetts Medical Society, Michigan State Medical Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: eMedicine Free access to materials Writing; MedLink Free access to materials Writing; Medicolegal defense work Consulting fee Consulting; Oakstone Publishing Payment Audio reviews

Brian Stettler, MD  Assistant Professor, Program Director, Emergency Medicine Residency Program, Department of Emergency Medicine, and Faculty Greater Cincinnati/Northern Kentucky Stroke Team, University of Cincinnati

Disclosure: Nothing to disclose.

Charles R Wira, MD  Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale School of Medicine

Charles R Wira, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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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 in this 70-year-old female with history of left-sided weakness for several hours duration.
Magnetic Resonance Imaging (MRI) was subsequently obtained in the same patient as in the above image. 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 magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
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 account for approximately one third of ischemic strokes.
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.
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 diffusion-weighted MRI (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.
MRI was obtained to evaluate this 62-year-old hypertensive and diabetic male with a 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 border-zone or watershed infarction, in this case the anterior and posterior 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.
This 48-year-old male 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 MCA and A2 segment of the right ACA (images courtesy of Concentric Medical).
Follow-up imaging in the same patient as in the above image after mechanical embolectomy demonstrates complete recanalization of the right middle cerebral artery and partial recanalization of the right A2 segment (images courtesy of Concentric Medical).
Cerebral angiogram demonstrates an occlusion of the distal basilar artery in this 31-year-old male approximately 4.5 hours after symptom onset (images courtesy of Concentric Medical).
Image on the left demonstrates deployment of a clot retrieval device in the same patient as in the above image. Follow up 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 CT in this 52-year-old male with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement 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.
MRA in the same patient as in the above image (left) demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal 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.
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 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 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 MCA with the apex representing the Sylvian point.
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.
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).
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 IV contrast. The information obtained from the dynamic parenchymal signal changes postcontrast is used to generate maps of different perfusion parameters.
Vascular distributions: MCA infarction. Noncontrast CT 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 (ACA territory), thalami and paramedian occipital lobe (PCA territory).
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 MCA.
Vascular distributions: 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 MCA distributions), greater on the left indicating multivessel involvement suggesting emboli.
Vascular distributions: 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.
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 MCA (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal and anterior temporal lobes, insula and basal ganglia. The ACA (blue) supplies the medial frontal and parietal lobes. The 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.
Table 1. Vascular Supply to the Brain
VASCULAR TERRITORYStructures Supplied
Anterior Circulation (Carotid)
Anterior Cerebral ArteryCortical branches: medial frontal and parietal lobe



Medial lenticulostriate branches: caudate head, globus pallidus, anterior limb of internal capsule



Middle Cerebral ArteryCortical branches: lateral frontal and parietal lobes lateral and anterior temporal lobe



Lateral lenticulostriate branches: globus pallidus and putamen, internal capsule



Anterior Choroidal ArteryOptic tracts, medial temporal lobe, ventrolateral thalamus, corona radiata, posterior limb of the internal capsule
Posterior Circulation (Vertebrobasilar)
Posterior Cerebral ArteryCortical branches: occipital lobes, medial and posterior temporal and parietal lobes



Perforating branches: brainstem, posterior thalamus and midbrain



Posterior Inferior Cerebellar ArteryInferior vermis; posterior and inferior cerebellar hemispheres
Anterior Inferior Cerebellar ArteryAnterolateral cerebellum
Superior Cerebellar ArterySuperior vermis; superior cerebellum
Table 2. NIH Stroke Scale
CategoryDescriptionScore
1alevel of consciousness (LOC)Alert



Drowsy



Stuporous



Coma



0



1



2



3



1bLOC questions (month, age)Answers both correctly



Answers 1 correctly



Incorrect on both



0



1



2



1cAnswers both correctly Answers 1 correctly Incorrect on bothObeys both correctly



Obeys 1 correctly



Incorrect on both



0



1



2



2Best gaze (follow finger)Normal



Partial gaze palsy



Forced deviation



0



1



2



3Best visual (visual fields)No visual loss



Partial hemianopia



Complete hemianopia



Bilateral hemianopia



0



1



2



3



4Facial palsy (show teeth, raise brows, squeeze eyes shut)Normal Minor



Partial Complete



0



1



2



3



5Motor arm left* (raise 90°, hold 10 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



6Motor arm right* (raise 90°, hold 10 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



7Motor leg left* (raise 30°, hold 5 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



8Motor leg right* (raise 30°, hold 5 seconds)No drift



Drift



Cannot resist gravity



No effort against gravity



No movement



0



1



2



3



4



9Limb ataxia (finger-nose, heel-shin)Absent



Present in 1 limb



Present in 2 limbs



0



1



2



10Sensory (pinprick to face, arm, leg)Normal



Partial loss



Severe loss



0



1



2



11Extinction/neglect (double simultaneous testing)No neglect



Partial neglect



Complete neglect



0



1



2



12Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty")Normal articulation



Mild to moderate dysarthria



Near to unintelligible or worse



0



1



2



13Best 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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