Ischemic Stroke in Emergency Medicine 

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

Background

Stroke is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Also previously called cerebrovascular accident (CVA) or stroke syndrome, stroke is a nonspecific term encompassing a heterogeneous group of pathophysiologic causes.

Broadly, however, strokes are classified as either hemorrhagic or ischemic. Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke. (Prior literature indicated that only 8-18% of strokes are hemorrhagic, but a retrospective review from a stroke center found that 40.9% of 757 strokes included in the study were hemorrhagic.[1] )

Based on the system of categorizing stroke developed in the multicenter Trial of Org 10172 in Acute Stroke Treatment (TOAST), ischemic strokes may be divided into the following 3 major subtypes[2] :

  • Large artery infarction: Thrombotic strokes are caused by in situ occlusions on atherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches.
  • Small-vessel, or lacunar, infarction
  • Cardioembolic infarction: Cardiogenic emboli are a common source of recurrent stroke. They may account for up to 20% of acute strokes and have been reported to have the highest 1-month mortality. (See Pathophysiology.)

The National Institute of Neurologic Disorders and Stroke (NINDS) recombinant tissue-type plasminogen activator (rt-PA) stroke study group first reported that the early administration of rt-PA benefited carefully selected patients with acute ischemic stroke.[3] The trial’s outcome led to the long-standing goal of t-PA administration within a 3-hour window for a patient deemed likely to benefit from thrombolytic intervention. Encouraged by this breakthrough study and the subsequent approval by the US Food and Drug Administration (FDA) of the use of t-PA in acute ischemic stroke, many medical professionals now consider acute ischemic stroke to be a medical emergency that may be amenable to treatment.

Thrombolytic therapy administered between 3 and 4.5 hours after the onset of symptoms was found to be efficacious in improving neurologic outcomes in the European Cooperative Acute Stroke Study III (ECASS III), suggesting a wider time window for the administration of thrombolytics.[4] Based on this and other data, in May 2009, the American Heart Association and the American Stroke Association guidelines for the administration of rt-PA were revised to expand the treatment window from 3 to 4.5 hours.[5] This indication has not yet been FDA approved.

Understanding of the pathophysiology, clinical presentation, and evaluation of the stroke patient is essential, as is knowledge of the therapeutic armamentarium currently available to treat acute ischemic stroke, which includes supportive care, treatment of neurologic complications, antiplatelet therapy, glycemic control, blood pressure control, prevention of hyperthermia, and thrombolytic therapy. (See Treatment and Management.) See the images below.

Axial noncontrast computed tomography (NCCT) demonAxial 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 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).
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Anatomy

The brain is the most metabolically active organ in the body. While representing only 2% of the body's mass, it requires 15-20% of the total resting cardiac output to provide the necessary glucose and oxygen for its metabolism.

Knowledge of cerebrovascular arterial anatomy and the territories supplied by each is useful in determining which vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate a diagnosis other than ischemic stroke, such as venous infarction.

Arterial distributions

The cerebral hemispheres are supplied by 3 paired major arteries, specifically, the anterior, middle, and posterior cerebral arteries.

The anterior and middle cerebral arteries carry the anterior circulation and arise from the supraclinoid internal carotid arteries. The anterior cerebral artery (ACA) supplies the medial portion of the frontal and parietal lobes and anterior portions of basal ganglia and anterior internal capsule. The middle cerebral artery (MCA) supplies the lateral portions of the frontal and parietal lobes, as well as the anterior and lateral portions of the temporal lobes, and gives rise to perforating branches to the globus pallidus, putamen and internal capsule.

The posterior cerebral arteries arise from the basilar artery and carry the posterior circulation. The posterior cerebral artery (PCA) gives rise to perforating branches that supply the thalami and brainstem and the cortical branches to the posterior and medial temporal lobes and occipital lobes. The cerebellar hemispheres are supplied inferiorly by the posterior inferior cerebellar artery (PICA) arising from the vertebral artery, superiorly by the superior cerebellar artery, and anterolaterally by the anterior inferior cerebellar artery (AICA) from the basilar artery.

The cerebral vasculature is seen in the images below. The images after Table 1 demonstrate cerebral artery infarction.

Frontal view of a cerebral angiogram with selectivFrontal 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). Lateral view of a cerebral angiogram illustrates tLateral 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.

Table 1. Vascular Supply to the Brain (Open Table in a new window)

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
The supratentorial vascular territories of the majThe 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. Vascular distributions: MCA infarction. NoncontrasVascular 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: ACA infarction. Diffusion-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 nonconVascular 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. Vascular distributions: anterior choroidal artery 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.
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Pathophysiology

Acute ischemic strokes are the result of vascular occlusion secondary to thromboembolic disease (see Etiology). Ischemia results in cell hypoxia and depletion of cellular adenosine triphosphate (ATP). Without ATP, energy failure results in an inability to maintain ionic gradients across the cell membrane and cell depolarization. With an influx of sodium and calcium ions and passive inflow of water into the cell, cytotoxic edema results.[6, 7, 8]

Ischemic core and penumbra

An acute vascular occlusion produces heterogeneous regions of ischemia in the affected vascular territory. The quantity of local blood flow is made up of any residual flow in the major arterial source and the collateral supply, if any.

Regions of the brain with CBF lower than 10 mL/100g of tissue/min are referred to collectively as the core, and these cells are presumed to die within minutes of stroke onset.

Zones of decreased or marginal perfusion (CBF < 25 mL/100g of tissue/min) are collectively called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours because of marginal tissue perfusion.

Ischemic cascade

On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and membrane ion-transport systems fail. The resulting influx of calcium leads to the release of a number of neurotransmitters, including large quantities of glutamate, which in turn activates N -methyl-D-aspartate (NMDA) and other excitatory receptors on other neurons. These neurons then become depolarized, causing further calcium influx, further glutamate release, and local amplification of the initial ischemic insult. This massive calcium influx also activates various degradative enzymes, leading to the destruction of the cell membrane and other essential neuronal structures.[9]

Free radicals, arachidonic acid, and nitric oxide are generated by this process, which leads to further neuronal damage.

Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown of the blood-brain barrier occurring within 4-6 hours after infarction. Following the barrier’s breakdown, proteins and water flood into the extracellular space, leading to vasogenic edema. Vasogenic edema produces greater levels of brain swelling and mass effect that peaks at 3-5 days and resolves over the next several weeks with resorption of water and proteins.[10, 11]

Within hours to days after a stroke, specific genes are activated, leading to the formation of cytokines and other factors that, in turn, cause further inflammation and microcirculatory compromise.[9] Ultimately, the ischemic penumbra is consumed by these progressive insults, coalescing with the infarcted core, often within hours of the onset of the stroke.

Infarction results in the death of astrocytes as well as the supporting oligodendroglia and microglia cells. The infarcted tissue eventually undergoes liquefaction necrosis and is removed by macrophages with the development of parenchymal volume loss. A well-circumscribed region of cerebrospinal fluid–like low density is eventually seen, consisting of encephalomalacia and cystic change. The evolution of these chronic changes may be seen in the weeks to months following the infarction.

Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage. This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence of thrombolytics. Hemorrhagic transformation is not always associated with neurologic decline and ranges from small petechial hemorrhages to hematomas requiring evacuation.

Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed producing petechial hemorrhage or more frank intraparenchymal hematoma.[6, 12, 13]

Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days post ictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.[6, 14, 3] Hemorrhagic transformation is also more likely following administration of t-PA, with noncontrast computed tomography (NCCT) scanning demonstrating areas of hypodensity.[15, 16, 17]

Poststroke cerebral edema and seizures

Although significant cerebral edema can occur after anterior circulation ischemic stroke, it is thought to be somewhat rare (10-20%).[18] Edema and herniation are the most common causes of early death in patients with hemispheric stroke.

Seizures occur in 2-23% of patients within the first days after stroke.[18] A fraction of patients who have experienced stroke develop chronic seizure disorders.

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Etiology

Ischemic strokes result from events that limit or stop blood flow, such as extracranial or intracranial thrombosis embolism, thrombosis in situ, or relative hypoperfusion. As blood flow decreases, neurons cease functioning, and irreversible neuronal ischemia and injury begin at blood flow rates of less than 18 mL/100 g of tissue/min.

Risk factors

Risk factors for ischemic stroke include modifiable and nonmodifiable etiologies. Identification of risk factors in each patient can uncover clues to the cause of the stroke and the most appropriate treatment and secondary prevention plan.

Nonmodifiable risk factors include the following:

  • Age
  • Race
  • Sex
  • Ethnicity
  • History of migraine headaches
  • Sickle cell disease
  • Fibromuscular dysplasia
  • Heredity

Modifiable risk factors include the following:

  • Hypertension (the most important)
  • Diabetes mellitus
  • Cardiac disease - Atrial fibrillation, valvular disease, mitral stenosis, and structural anomalies allowing right to left shunting, such as a patent foramen ovale and atrial and ventricular enlargement
  • Hypercholesterolemia
  • Transient ischemic attacks (TIAs)
  • Carotid stenosis
  • Hyperhomocystinemia
  • Lifestyle issues - Excessive alcohol intake, tobacco use, illicit drug use, obesity, physical inactivity
  • Oral contraceptive use

Among the types of cardiac disease that increase stroke risk are atrial fibrillation, valvular disease, mitral stenosis, and structural anomalies allowing right-to-left shunting, such as a patent foramen ovale and atrial and ventricular enlargement.

TIA is a transient neurologic deficit with no evidence of an ischemic lesion on neuroimaging. Roughly 80% resolve within 60 minutes.[19]

TIA can result from the aforementioned mechanisms of stroke. Data suggest that roughly 10% of patients with TIA suffer stroke within 90 days and half of these patients suffer stroke within 2 days.[20, 21]

Genetic and inflammatory mechanisms

Evidence continues to accumulate to suggest important roles for inflammation and genetic factors in the process of atherosclerosis and, specifically, in stroke. According to the current paradigm, atherosclerosis is not a bland cholesterol storage disease, as previously thought, but a dynamic, chronic, inflammatory condition caused by a response to endothelial injury. Traditional risk factors, such as oxidized low-density lipoprotein (LDL) and smoking, contribute to this injury. It has been suggested, however, that infections may also contribute to endothelial injury and atherosclerosis.

Host genetic factors, moreover, may modify the response to these environmental challenges, although inherited risk for stroke is likely multigenic. Even so, specific single-gene disorders with stroke as a component of the phenotype demonstrate the potency of genetics in determining stroke risk.

For more information, see Genetic and Inflammatory Mechanisms in Stroke. In addition, complete information on the following metabolic disease and stroke can be found in the main articles:

Flow disturbances

Stroke symptoms can result from inadequate cerebral blood flow due to decreased blood pressure (and specifically, decreased cerebral perfusion pressure) or as a result of hematologic hyperviscosity due to sickle cell disease or other hematologic illnesses, such as multiple myeloma and polycythemia vera. In these instances, cerebral injury may occur in the presence of damage to other organ systems.

For more information, see Blood Dyscrasias and Stroke.

Large-artery occlusion

Large-artery occlusion typically results from embolization of atherosclerotic debris originating from the common or internal carotid arteries or from a cardiac source. A smaller number of large-artery occlusions may arise from plaque ulceration and in situ thrombosis. Large-vessel ischemic strokes more commonly affect the MCA territory with the ACA territory affected to a lesser degree. (See the images below.)

Noncontrast CT in this 52-year-old male with a hisNoncontrast 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 (lefMRA 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. MIP image from a CTA demonstrates a filling defectMIP 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.

Lacunar strokes

Lacunar strokes represent 13-20% of all ischemic strokes. They occur when the penetrating branches of the MCA, the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery become occluded. (See the image below.)

Axial noncontrast CT demonstrates a focal area of 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.

Causes of lacunar infarcts include the following:

  • Microatheroma
  • Lipohyalinosis
  • Fibrinoid necrosis secondary to hypertension or vasculitis
  • Hyaline arteriosclerosis
  • Amyloid angiopathy

The great majority are related to hypertension.

Embolic strokes

Cardiogenic emboli may account for up to 20% of acute strokes.

Emboli may arise from the heart, the extracranial arteries, or, rarely, the right-sided circulation (paradoxical emboli) with subsequent passage through a patent foramen ovale. The sources of cardiogenic emboli include the following:

MI is associated with a 2-3% incidence of embolic strokes, of which 85% occur in the first month after MI.[22] Embolic strokes tend to have a sudden onset, and neuroimaging may demonstrate previous infarcts in several vascular territories or calcific emboli.

Risk factors include atrial fibrillation and recent cardiac surgery. Cardioembolic strokes may be isolated, multiple and in a single hemisphere, or scattered and bilateral; the latter 2 types indicate multiple vascular distributions and are more specific for cardioembolism. Multiple and bilateral infarcts can be the result of embolic showers or recurrent emboli. Other possibilities for single and bilateral hemispheric infarctions include emboli originating from the aortic arch and diffuse thrombotic or inflammatory processes that can lead to multiple small-vessel occlusions.[23, 24] (See the image below.)

Cardioembolic stroke: Axial diffusion-weighted imaCardioembolic 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.

For more information, see Cardioembolic Stroke.

Thrombotic strokes

Thrombogenic factors may include injury to and loss of endothelial cells, exposing the subendothelium, and platelet activation by the subendothelium, activation of the clotting cascade, inhibition of fibrinolysis, and blood stasis. Thrombotic strokes are generally thought to originate on ruptured atherosclerotic plaques. Arterial stenosis can cause turbulent blood flow, which can increase the risk for thrombus formation, atherosclerosis (ie, ulcerated plaques), and platelet adherence; all cause the formation of blood clots that either embolize or occlude the artery.

Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis. In other patients, especially younger patients, other causes should be considered, including the following[25, 6] :

Hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein S deficiency, pregnancy)

  • Sickle cell disease
  • Fibromuscular dysplasia
  • Arterial dissections
  • Vasoconstriction associated with substance abuse

Watershed infarcts

Vascular watershed, or border-zone, infarctions occur at the most distal areas between arterial territories. They are believed to be secondary to embolic phenomenon or due to severe hypoperfusion, such as in carotid occlusion or prolonged hypotension.[26, 27, 28]

MRI was obtained to evaluate this 62-year-old hypeMRI 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.
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Epidemiology

Stroke is the leading cause of disability and the third leading cause of death in the United States.[29]

More than 700,000 persons per year suffer a first-time stroke in the United States, with 20% of these individuals dying within the first year after the stroke. If current trends continue, this number is projected to reach 1 million per year by the year 2050.[30]

The global incidence of stroke is unknown.

Stroke incidence by race and sex

In the United States, blacks have an age-adjusted risk of death from stroke that is 1.49 times that of whites.[31]

Hispanics have a lower overall incidence of stroke than whites and blacks but more frequent lacunar strokes and stroke at an earlier age.

Men are at higher risk for stroke than women; white males have a stroke incidence of 62.8 per 100,000, with death being the final outcome in 26.3% of cases, while women have a stroke incidence of 59 per 100,000 and a death rate of 39.2%.

Stroke and age

Although stroke often is considered a disease of elderly persons, one third of strokes occur in persons younger than 65 years.[30] Risk of stroke increases with age, especially in patients older than 64 years, in whom 75% of all strokes occur.

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Prognosis

The prognosis after acute ischemic stroke varies greatly, depending on the stroke severity and on the patient’s premorbid condition, age, and poststroke complications.[2]

Some patients experience hemorrhagic transformation of their infarct (See Pathophysiology). This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence of thrombolytics. Hemorrhagic transformation is not always associated with neurologic decline and ranges from small petechial hemorrhages to hematomas requiring evacuation.

In the Framingham and Rochester stroke studies, the overall mortality rate at 30 days after stroke was 28%, the mortality rate at 30 days after ischemic stroke was 19%, and the 1-year survival rate for patients with ischemic stroke was 77%.

In the United States, 20% of individuals die within the first year after a first-time stroke, as previously mentioned.

Cardiogenic emboli are associated with the highest 1-month mortality in patients with acute stroke.

In stroke survivors from the Framingham Heart Study, 31% needed help caring for themselves, 20% needed help when walking, and 71% had impaired vocational capacity in long-term follow-up.

The presence of CT scan evidence of infarction early in presentation has been associated with poor outcome and with an increased propensity for hemorrhagic transformation after thrombolytics.[3, 32, 33]

Acute ischemic stroke has been associated with acute cardiac dysfunction and arrhythmia, which then correlate with worse functional outcome and morbidity at 3 months.

Data suggest that severe hyperglycemia is independently associated with poor outcome and reduced reperfusion in thrombolysis, as well as extension of the infarcted territory.[34, 35, 36]

To see complete information on Motor Recovery in Stroke, please go to the main article by clicking here.

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Patient Education

Public education must involve all age groups. Incorporating stroke into basic life support (BLS) and cardiopulmonary resuscitation (CPR) curricula is just one way to reach a younger audience. Avenues to reach an audience with a higher stroke risk include using local churches, employers, and senior organizations to promote stroke awareness.

The American Stroke Association advises the public to be aware of the symptoms of stroke that are easily recognized and to call 911 immediately. These symptoms include the following:

  • Sudden numbness or weakness of face, arm, or leg, especially on 1 side of the body
  • Sudden confusion
  • Sudden difficulty in speaking or understanding
  • Sudden deterioration of vision in 1 or both eyes
  • Sudden difficulty in walking, dizziness, and loss of balance or coordination
  • Sudden, severe headache with no known cause

For excellent patient education resources, visit eMedicine's Stroke Center and Dementia Center. In addition, see eMedicine's patient education articles Stroke, Transient Ischemic Attack (Mini-stroke),and Stroke-Related Dementia.

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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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