Sections

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Diagnostic Considerations

Stroke mimics commonly confound the clinical diagnosis of stroke. One study reported that 19% of patients diagnosed with acute ischemic stroke by neurologists before cranial CT scanning actually had non-cerebrovascular causes for their symptoms.

The most frequent stroke mimics include the following:

Seizure (17%)
Systemic infection (17%)
Brain tumor (15%)
Toxic-metabolic disorders, such as hyponatremia and hypoglycemia (13%)
Positional vertigo (6%)
Conversion disorder

In the prehospital and Emergency Department (ED) settings, hypoglycemia is a common stroke mimic and is particularly important to consider, since it can be readily detected and corrected.^{[60, 61]}For more information, see Hyperglycemia and Hypoglycemia in Stroke.

Ischemic versus hemorrhagic stroke

Although the definitive distinction of ischemic stroke from hemorrhagic stroke requires neuroimaging, a meta-analysis found that the following clinical findings increase the probability of hemorrhagic stroke^[62]:

Coma (likelihood ratio [LR] 6.2)
Neck stiffness (LR 5.0)
Seizures accompanying the neurologic deficit (LR 4.7)
Diastolic blood pressure >110 mm Hg (LR 4.3)
Vomiting (LR 3.0)
Headache (LR 2.9)

Findings that decrease the probability of hemorrhage include cervical bruit (LR 0.12) and prior transient ischemic attack (LR 0.34).

Transient ischemic attack

Transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction that results from focal cerebral, spinal cord, or retinal ischemia and is not associated with acute tissue infarction. Roughly 80% of TIAs resolve within 60 minutes.^[63]TIA can result from the same mechanisms as ischemic stroke. Data suggest that roughly 10% of patients with TIA will suffer a stroke within 90 days and of those, half suffer a stroke within 2 days.^{[64, 65]}

The classic definition of TIA included symptoms lasting as long as 24 hours. With advances in neuroimaging, however, it now appears that many such cases presumed to be TIA actualy are minor strokes with areas of infarction found on imaging but with resolved symptoms, rather than true TIAs. Thus, the current definition of TIA is based on tissue pathophysiology rather than symptom duration.^[63]

Cerebral venous thrombosis

Diagnosis and management of a rare form of stroke, cerebral venous thrombosis (CVT), was the subject of a 2011 American Heart Association/American Stroke Association (AHA/ASA) statement for healthcare professionals. According to the statement, diagnosing CVT requires a high degree of clinical suspicion. Most people diagnosed with CVT present with headache, often of increasing severity and usually accompanied by focal neurologic signs.^[51]

Differentials

Bell Palsy

Brain Neoplasms

Conversion Disorder in Emergency Medicine

Hemorrhagic Stroke

Hypoglycemia

Migraine Headache

Seizure Assessment in the Emergency Department

Emergent Management of Subarachnoid Hemorrhage

Syncope

Transient Global Amnesia

Workup

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Media Gallery

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.
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.
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.
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.
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.
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.
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.
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.
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).
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).
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.
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).
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).
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.
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.
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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Table 1. Vascular Supply to the Brain

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

Table 2. National Institutes of Health Stroke Scale

Category

Description

Score

level of consciousness (LOC)

Alert

Drowsy

Stuporous

Coma

LOC questions (month, age)

Answers both correctly

Answers 1 correctly

Incorrect on both

LOC commands (open and close eyes,

grip and release nonparetic hand)

Obeys both correctly

Obeys 1 correctly

Incorrect on both

Best gaze (follow finger)

Normal

Partial gaze palsy

Forced deviation

Best visual (visual fields)

No visual loss

Partial hemianopia

Complete hemianopia

Bilateral hemianopia

Facial palsy (show teeth, raise brows,

squeeze eyes shut)

Normal

Minor

Partial

Complete

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

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

Motor leg left* (raise 30°, hold 5 seconds)

No drift

Drift

Cannot resist gravity

No effort against gravity

No movement

Motor leg right* (raise 30°, hold 5 seconds)

No drift

Drift

Cannot resist gravity

No effort against gravity

No movement

Limb ataxia (finger-nose, heel-shin)

Absent

Present in 1 limb

Present in 2 limbs

Sensory (pinprick to face, arm, leg)

Normal

Partial loss

Severe loss

Extinction/neglect (double simultaneous testing)

No neglect

Partial neglect

Complete neglect

Dysarthria (speech clarity to "mama,

baseball, huckleberry, tip-top, fifty-fifty")

Normal articulation

Mild to moderate dysarthria

Near to unintelligible or worse

Best language** (name items,

describe pictures)

No aphasia

Mild to moderate aphasia

Severe aphasia

Mute

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)

Back to List

Author

Edward C Jauch, MD, MBA, MS, FAHA, FACEP Chair, Department of Research, University of North Carolina Health Sciences at MAHEC; Professor (Adjunct), Departments of Emergency Medicine and Neurology, University of North Carolina at Chapel Hill School of Medicine

Edward C Jauch, MD, MBA, MS, FAHA, FACEP is a member of the following medical societies: American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Sami Al Kasab, MD Assistant Professor of Neurology and Neurosurgery, Department of Neurosurgery, Medical University of South Carolina College of Medicine

Sami Al Kasab, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians, American Heart Association

Disclosure: Nothing to disclose.

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.

Chief Editor

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

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

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Abbott Laboratories, advisory group.

Acknowledgements

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