Ischemic Stroke in Emergency Medicine Clinical Presentation

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

History

A focused medical history for patients with ischemic stroke aims to identify risk factors for atherosclerotic and cardiac disease, including hypertension, diabetes mellitus, tobacco use, high cholesterol, and a history of coronary artery disease, coronary artery bypass, or atrial fibrillation (see Etiology). Consider stroke in any patient presenting with acute neurologic deficit or any alteration in level of consciousness. Common signs of stroke include the following:

  • Acute hemiparesis or hemiplegia
  • Acute hemisensory loss
  • Complete or partial hemianopia, monocular or binocular visual loss, or diplopia
  • Dysarthria or aphasia
  • Ataxia, vertigo, or nystagmus
  • Sudden decrease in consciousness

In younger patients, elicit a history of recent trauma, coagulopathies, illicit drug use (especially cocaine), migraines, or use of oral contraceptives.

Establishing the time at which the patient was last without stroke symptoms is especially critical when thrombolytic therapy is an option. If the patient awakens with symptoms, then the time of onset is defined as the time at which the patient was last seen to be without symptoms. Family members, coworkers, and bystanders may be required to help establish the exact time of onset, especially in right hemispheric strokes accompanied by neglect or left hemispheric strokes with aphasia.

Next

Physical Examination

The goals of the physical examination include detecting extracranial causes of stroke symptoms, distinguishing stroke from stroke mimics, determining and documenting for future comparison the degree of deficit, and localizing the lesion.

The physical examination always includes a careful head and neck examination for signs of trauma, infection, and meningeal irritation.

Stroke should be considered in any patient presenting with an acute neurologic deficit (focal or global) or altered level of consciousness. No historical feature distinguishes ischemic from hemorrhagic stroke, although nausea, vomiting, headache, and change in level of consciousness are more common in hemorrhagic strokes.

Common symptoms of stroke include the following:

  • Abrupt onset of hemiparesis, monoparesis, or quadriparesis
  • Hemisensory deficits
  • Monocular or binocular visual loss
  • Visual field deficits
  • Diplopia
  • Dysarthria
  • Ataxia
  • Vertigo
  • Aphasia
  • Sudden decrease in the level of consciousness

Although such symptoms can occur alone, they are more likely to occur in combination.

A careful search for the cardiovascular causes of stroke requires examination of the ocular fundi (retinopathy, emboli, hemorrhage), heart (irregular rhythm, murmur, gallop), and peripheral vasculature (palpation of carotid, radial, and femoral pulses, auscultation for carotid bruit).

Patients with a decreased level of consciousness should be assessed to ensure that they are able to protect their airway.

The physical examination must encompass all of the major organ systems, starting with the airway, breathing, and circulation (ABC) and the vital signs. Patients with stroke, especially hemorrhagic stroke, can clinically deteriorate quickly; therefore, constant reassessment is critical. Ischemic strokes, unless large or involving the brainstem, do not tend to cause immediate problems with airway patency, breathing, or circulation compromise. On the other hand, patients with intracerebral or subarachnoid hemorrhage frequently require intervention for airway protection and ventilation.

Vital signs, while nonspecific, can point to impending clinical deterioration and may assist in narrowing the differential diagnosis. Many patients with stroke are hypertensive at baseline, and their blood pressure may become more elevated after stroke. While hypertension at presentation is common, blood pressure decreases spontaneously over time in most patients. Acutely lowering blood pressure has not proven to be beneficial in these stroke patients in the absence of signs and symptoms of associated malignant hypertension, acute myocardial infarction, CHF, or aortic dissection.

Head and neck examination

A careful examination of the head and neck is essential. Contusions, lacerations, and deformities may suggest trauma as the etiology for the patient's symptoms. Auscultation of the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.

Cardiac examination

Cardiac arrhythmias, such as atrial fibrillation, are found commonly in patients with stroke. Similarly, strokes may occur concurrently with other acute cardiac conditions, such as acute myocardial infarction and acute CHF; thus, auscultation for murmurs and gallops is recommended.

Examination of the extremities

Carotid or vertebrobasilar dissections and, less commonly, thoracic aortic dissections may cause ischemic stroke. Unequal pulses or blood pressures in the extremities may reflect the presence of aortic dissections.

Neurologic examination

With the availability of thrombolytic therapy for acute ischemic stroke in selected patients, the physician must be able to perform a brief, but accurate, neurologic examination on patients with suspected stroke syndromes. The goals of the neurologic examination include the following:

  • Confirming the presence of a stroke syndrome (to be defined further by cranial computed tomography [CT] scanning)
  • Distinguishing stroke from stroke mimics
  • Establishing a neurologic baseline should the patient's condition improve or deteriorate

Essential components of the neurologic examination include the evaluation of cranial nerves, motor function, sensory function, cerebellar function, gait, and deep tendon reflexes, as well as of mental status and level of consciousness. The skull and spine also should be examined, and signs of meningismus should be sought.

Central facial weakness from a stroke should be differentiated from the peripheral weakness of Bell palsy. With peripheral lesions (Bell palsy), the patient is unable to lift the eyebrows, wrinkle the forehead, or or close the eye on the affected side.

A useful tool in quantifying neurological impairment is the National Institutes of Health Stroke Scale (NIHSS). The NIHSS (see Table 2, below) is used mostly by stroke teams. It enables the consultant to rapidly determine the severity and possible location of the stroke. A patient's score on the NIHSS is strongly associated with outcome, and it can help to identify those patients who are likely to benefit from thrombolytic therapy and those who are at higher risk of developing hemorrhagic complications of thrombolytic use.

This scale is easily used and focuses on the following 6 major areas of the neurologic examination:

  • level of consciousness
  • Visual function
  • Motor function
  • Sensation and neglect
  • Cerebellar function
  • Language

The NIHSS is a 42-point scale, with minor strokes usually being considered to have a score less than 5. An NIHSS score greater than 10 correlates with an 80% likelihood of visual flow deficits on angiography. However, discretion must be used in assessing the magnitude of the clinical deficit; for instance, if a patient's only deficit is being mute, the NIHSS score will be 3. Additionally, the scale does not measure some deficits associated with posterior circulation strokes (ie, vertigo, ataxia).[37]

Table 2. NIH Stroke Scale (Open Table in a new window)

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)



Middle cerebral artery stroke

MCA occlusion commonly produces contralateral hemiparesis, contralateral hypesthesia, ipsilateral hemianopsia, and gaze preference toward the side of the lesion. Agnosia is common, and receptive or expressive aphasia may result if the lesion occurs in the dominant hemisphere. Neglect, inattention, and extinction of double simultaneous stimulation may occur in nondominant hemisphere lesions. Since the MCA supplies the upper extremity motor strip, weakness of the arm and face is usually worse than that of the lower limb.

Anterior cerebral artery stroke

ACA occlusions primarily affect frontal lobe function and can result in disinhibition and speech perseveration, producing primitive reflexes (eg, grasping, sucking reflexes), altered mental status, impaired judgment, contralateral weakness (greater in legs than arms), contralateral cortical sensory deficits gait apraxia, and urinary incontinence.

Posterior cerebral artery stroke

PCA occlusions affect vision and thought, producing contralateral homonymous hemianopsia, cortical blindness, visual agnosia, altered mental status, and impaired memory.

Vertebrobasilar artery occlusions are notoriously difficult to detect because they cause a wide variety of cranial nerve, cerebellar, and brainstem deficits. These include the following:

  • Vertigo
  • Nystagmus
  • Diplopia
  • Visual field deficits
  • Dysphagia
  • Dysarthria
  • Facial hypesthesia
  • Syncope
  • Ataxia

A hallmark of posterior circulation stroke is that there are crossed findings: ipsilateral cranial nerve deficits and contralateral motor deficits. This is contrasted to anterior stroke, which produces only unilateral findings.

Lacunar stroke

Lacunar strokes result from occlusion of the small, perforating arteries of the deep subcortical areas of the brain. The infarcts are generally from 2-20 mm in diameter. The most common lacunar syndromes include pure motor, pure sensory, and ataxic hemiparetic strokes. By virtue of their small size and well-defined subcortical location, lacunar infarcts do not lead to impairments in cognition, memory, speech, or level of consciousness.

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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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