Stroke

Asma M. Moheet
Irene Katzan
Published: September 2013
Contents

Definition and Etiology

A stroke is defined as an acute loss of neurological function due to an abnormal perfusion of
brain tissue. Most strokes are ischemic (87%) in nature and commonly result from an arterial
obstruction by a thrombus or embolus. Hemorrhagic strokes (13%) are caused by rupture or leak
of a blood vessel either within the primary brain tissue or subarachnoid space. This chapter
provides a clinical approach to the evaluation and management of stroke, with a focus on
ischemic stroke.
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Prevalence and Risk Factors

Because stroke is the leading cause of morbidity and the fourth-leading cause of death in the
United States today, optimal reduction of risk factors is paramount in preventing and managing
stroke. Modifiable and nonmodifiable stroke risk factors are listed in Table 1. In 2005, the
prevalence of stroke in noninstitutionalized adults was 5.8 million in the United States alone.
Based on American Stroke Association data, the estimated direct and indirect cost of stroke for
2008 was $65.5 billion, with an estimated lifetime cost of $140,000 per patient.
Table 1: Cerebrovascular Disease Risk Factors
Disease
Ischemic stroke

Modifiable
Hypertension
Diabetes
Atrial fibrillation
Smoking
Hyperlipidemia
Carotid stenosis
Lack of physical
activity

Not Modifiable
Age >55
Male gender
Black race
Family
history of
stroke
Personal
history of
stroke

Hypertension
Antithrombotic
use
Thrombolytic use
Coagulopathy

Illicit Drug Use

Intraparenchymal
hemorrhage

Subarachnoid
hemorrhage

Hypertension
Smoking

Alcohol Abuse

Sickle Cell
Disease
Vascular
malformatio
n
Amyloid
angiopathy
Neoplasm
Trauma
Acute
ischemic
stroke
Aneurysm
Family
history of
aneurysm or
connective
tissue
disease
Black or
Hispanic
Race
Other
vascular
malformatio
n
Trauma
Female
gender

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Pathophysiology and Natural History

Ischemic Stroke
The mechanism of stroke is an important characteristic of ischemic strokes and help predict
outcomes after stroke and assess risk of stroke recurrence. Based on prior clinical trials, a
subclassification scheme of five etioloiges of ischemic stroke has become widely accepted. They
are large-artery atherosclerosis, embolism, small-vessel disease, stroke of other determined
etiology, and stroke of undetermined etiology.

Large-Artery Atherosclerosis
High-grade stenosis or occlusion of the major intra- and extra-cranial arteries, which include the
internal carotid artery, the vertebral artery, the basilar artery, and other major branches of the
circle of Willis, occur due to deposition of plaque and may lead to a flow-dependent state of
perfusion. With interruption of flow due to acute plaque rupture or a prolonged low-flow state
due to relative hypotension, a loss of adequate cerebral perfusion results in ischemia and focal
neurologic deficit. A more common cause of stroke in the setting of large-artery atherosclerosis is
the formation of thrombus that can block flow directly or dislodge to form an atheroembolism
that obstructs a distal vessel.
Cardiac Embolism
Turbulent or stagnant flow states in the heart can result in formation of thrombi. These thrombi
can dislodge and occlude blood vessels in the intracranial circulation farther downstream. The
most common cause of cardioembolic stroke is atrial fibrillation. Other causes include severe left
ventricular dysfunction resulting in a low ejection fraction, paradoxical embolus from the venous
system due to a shunt through a septal defect such as an aneurysm or patent foramen ovale, or
vessel-to-vessel atheroembolism due to atherosclerotic disease in the vertebral arteries, carotid
arteries, and aortic arch.
Small-Vessel Disease
Changes in the arterial vasculature of small perforating arteries can result in narrowing of the
vessel lumen and eventual occlusion. Chronic hypertension is one state that leads to vessel
damage secondary to lipohyalinosis and endothelial damage. Hyperlipidemia, smoking, and
diabetes also lead to changes in the vessel wall that result in decreased compliance and
intraluminal stenosis. These changes often result in lacunar infarcts, which are small infarcts
defined by their size (<15 mm3) and are typically located in deep structures such as the internal
capsule, basal ganglia, thalamus, and pons.
Stroke of Other Determined Etiology
The majority of ischemic strokes are classified in one of the previous categories. Rarely, other
causes must be investigated, particularly in patients who are young and have no risk factors for
stroke. Among these causes are coagulopathies, vasculopathies, genetic disorders, and metabolic
disorders.
Stroke of Undetermined Etiology
In a significant number of cases (40%), no clear explanation can be found for an ischemic
stroke despite an extensive diagnostic evaluation. These strokes are classified as strokes of
undetermined etiology, or cryptogenic strokes. This is a diagnosis of exclusion, however, and

should only be made once a thorough search for both common and uncommon causes of stroke
has been completed.
Transient Ischemic Attack
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by focal
brain or retinal ischemic, with clinical symptoms typically lasting less than one hour, and without
evidence of acute infarction. It is important to note that many patients with transient symptoms
lasting less than 24 hours actually have associated infarction on imaging and should be classified
as a stroke. Patients with TIA or mild stroke are at risk for developing stroke in the near future:
10% to 15% of patients will have a stroke within 3 months, with half occurring within 48 hours.
Intracerebral Hemorrhage
Intracerebral hemorrhage occurs when a blood vessel within the brain parenchyma ruptures and
causes accumulation of blood within the brain tissue. Weakening of the blood vessel wall is often
a result of chronic uncontrolled hypertension or a problem intrinsic to the blood vessel such as
amyloid angiopathy or other vascular malformation. In hypertension, microaneurysms in
perforating vessels, known as Charcot-Bouchard aneurysms, can rupture and cause bleeding. The
thalamus, basal ganglia, pons, and cerebellum are the most common sites for these hypertensive
bleeds. Lobar hemorrhages more commonly result from amyloid angiopathy, which is typically
seen in older patients. This should be suspected when there is evidence of prior areas of
hemorrhage manifested as hemosiderin deposits on magnetic resonance imaging (MRI). Other
causes of intracerebral hemorrhage include the use of anticoagulants, thrombolytics, and
antiplatelet agents, particularly when levels are supratherapeutic. They may also be caused by an
underlying primary or metastatic brain tumor, especially when there are focal areas of necrosis
within the tumor bed.
Subarachnoid Hemorrhage
Subarachnoid hemorrhage is most commonly due to trauma and typically occurs adjacent to
areas of bony prominence, such as the temporal poles and the frontal poles. Subarachnoid
hemorrhage can also result from rupture of a cerebral aneurysm. Aneurysms are usually located
at vulnerable branch points in the circle of Willis due to weakening of the vessel wall. The most
common sites of aneurysm formation and rupture are in the distribution of the anterior
communicating artery and the posterior communicating artery. Uncontrolled chronic
hypertension, smoking, and a family history of aneurysms are risk factors for formation and
rupture of aneurysms. In 10% to 20% of cases of spontaneous, nontraumatic subarachnoid
hemorrhage, no cause is found despite serial angiography. The prognosis for these patients is
typically favorable.
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Signs and Symptoms

An acute stroke is signified by a sudden onset of focal neurologic deficit and is variable
depending on the area of tissue ischemia. Localization can often be made by the pattern of
clinical findings. Common stroke syndromes are listed in Table 2 according to vascular
distribution. Although headache might accompany an ischemic stroke, an acute and severe
headache that is maximal at onset more commonly represents a subarachnoid or
intraparenchymal hemorrhage, especially if this is followed by somnolence or decreased mental
status. Seizures can also occur at the onset of ischemic or hemorrhagic strokes.
Table 2: Overview of Selected Stroke Syndromes
Vascular
Territory
Anterior
cerebral artery

Middle
cerebral artery

Posterior
cerebral artery

Area Affected
Frontal pole and
mesial
lobe

temporal, parietal
lobes

Occipital lobe

syndrome

pontine

artery

Basilar artery
Vertebral

Frontal signs such as abulia

Contralateral: face and arm > leg
weakness, sensory loss to all modalities,
visual field cut, visual-spatial neglect
Ipsilateral: gaze preference

cerebellar

artery

Lateral

cerbellar

Contralateral: leg > face and arm

weakness

Posterior frontal,

inferior

inferior

frontal

Anterior

Posterior

Signs and Symptoms

Lateral

medulla

Dominant hemisphere affected: aphasia,

alexia, agraphia, acalculia
Contralateral: homonymous hemianopia

With thalamic involvement: Sensory loss

to all modalities or pain

Contralateral: hemiparesis and

hemisensory loss of pain and temperature

Ipsilateral: ataxia

Contralateral: hemibody pain and

temperature loss
Ipsilateral: facial pain, hemifacial pain
and temperature loss, ataxia, nystagmus,
nausea/vomiting, vertigo, Horner's
syndrome, dysphagia

(Wallenberg
syndrome)

Hiccups
Bilateral: progressive quadriplegia, facial
weakness

syndrome)

Medial medulla

Lateral gaze weakness with sparing of

vertical gaze
Contralateral: hemibody weakness, loss

Pons

(locked-in

of vibration and proprioception

artery
Vertebral
artery

Lateral medulla

Ipsilateral: tongue weakness and/or

atrophy

Wallenberg syndrome

Motor symptoms consist of facial droop, hemiparesis, or isolated weakness of the arm or leg.
Dizziness, slurred speech, problems with coordination, or difficulty with gait and balance may
also be reported and may be due to involvement of cerebellar fibers. Sensory symptoms include
numbness or altered sensation, with tingling paresthesias of one side of the body or face, or both.
Vision loss in one eye or both eyes as in a homonymous hemianopsia can also occur.
Patients with an acute stroke might also present with confusion or are sometimes
perceived as being confused when there is an expressive or receptive aphasia or
a visuospatial neglect phenomenon.
One of the most urgent and potentially devastating stroke syndromes is thrombosis of the basilar
artery, which can manifest with acute quadriparesis, loss of consciousness, and respiratory
failure.
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Diagnosis
The first step in correctly identifying a stroke is a rapid, thorough neurologic assessment
consisting of a focused history and neurologic examination. A differential diagnosis is listed in
Box 1. It is of utmost importance to establish a time of symptom onset when eliciting the history
from the patient or witnesses. If the patient woke with symptoms, treatment is based on the time
the patient was last seen normal, which for many would be when they went to bed the night
before.
Box 1: Differential Diagnosis of Stroke
Complex or atypical migraine
Conversion disorder
Electrolyte disturbance
Hypoglycemia or hyperglycemia
Intracranial neoplasm
Meningitis, encephalitis, or systemic infection
Multiple sclerosis exacerbation
Seizure
Subdural hemorrhage

Vital signs should be assessed frequently, with particular attention to blood pressure and heart
rate. It is also necessary to obtain a blood glucose level immediately because both hypo- and
hyperglycemia can manifest clinically with acute neurologic deficits, mimicking a stroke.
Regarding the physical examination, a variety of tools in the form of validated scales are
available for evaluation of the patient at presentation. The NIH Stroke Scale is a widely accepted
and useful tool that is recommended in the acute phase for the purpose of quickly identifying
focal neurologic deficits and their severity (Class I, Level B recommendation).

Treatment
Acute Management and Interventions
The first step in the appropriate management of acute stroke is early identification at symptom
onset. Early notification of emergency medical services with use of stroke-identification
algorithms, management in the field with stroke protocols, and emergent transport to the nearest
center capable of treating acute stroke is recommended (Class I, Level B evidence). Airway,
breathing, and circulation should be stabilized, with airway support and ventilatory assistance in
the appropriate patients (Class I, Level C evidence). Initial laboratory testing and CT brain scan
should be performed as detailed earlier.
In patients who present with stroke symptoms within 3 hours of 'last known well' and who meet
eligibility criteria (Box 2), treatment with IV recombinant tissue plasminogen activator (rtPA) is
recommended at a dose of 0.9 mg/kg (maximum dose, 90 mg) over 1 hour, with the first 10%
given as a bolus over 1 minute (Class I, Level A evidence). Studies have demonstrated that 31%
to 50% of patients treated with rtPA within 3 hours experienced improved recovery at 3 months
as compared to 20% to 38% of patients in the placebo arm. However, strict adherence to national
guidelines in the administration of rtPA and postlysis management is critical, given the 6% risk
of intracranial hemorrhage. The time window for IV rtPA has been expanded more recently out
to 4.5 hours from time last known well. (Class I, Level B evidence) based upon a European study
The European Cooperative Acute Study III (ECASS III). In this study, 52.4% of subjects
receiving IV rtPA within 3 to 4.5 hours had favorable outcome compared to 45.2% of subjects
that received placebo. The eligibility criteria for treatment in the 3- to 4.5-hour time period are
similar to those for persons treated at earlier time periods, but with the additional exclusion
criteria (See Box 2). Although the 3- to 4.5-hour time period has been endorsed by the American
Stroke Association, it has not yet been approved by the Food and Drug Administration (FDA).
Box 2: Exclusion Criteria for Treatment of Acute Ischemic Stroke with rtPA within 3 Hours
of Last Known Well
Onset of symptoms >3 hours
CT with acute hemorrhage or hypodensity involving >1/3 of the hemisphere
Systolic blood pressure >185 mm Hg and diastolic blood pressure >110 mm Hg
Evidence of active bleeding or acute trauma on exam
Anticoagulant therapy with INR >1.7 (or elevated PTT if receiving heparin)
Platelet count <100,000 mm3

Blood glucose <50 mg/dL

Seizure at symptom onset
History of prior intracranial hemorrhage, neoplasm, or vascular malformation
Head trauma or stroke in past 3 months
Myocardial infarction in past 3 months
Gastrointestinal or urinary tract hemorrhage in past 3 weeks
Major surgery in past 14 days
Arterial puncture at a noncompressible site in past 7 days
Rapid, spontaneous improvement of neurologic signs
Symptoms suggesting subarachnoid hemorrhage
Mild neurologic deficit
Additional Exclusion Criteria for Treatment within 3 to 4.5 Hours of Last Known Well
Age >80 years
Taking oral anticoagulants regardless of INR level Baseline NIHSS >25
History of both stroke and diabetes
CT, computed tomography; INR, international normalized ratio; PTT, partial thromboplastin
time; rtPA, recombinant tissue plasminogen activator; NIHSS, National Institutes of Health
Stroke Scale.
In selected patients who are not candidates for IV rtPA therapy, intra-arterial thrombolysis by a
qualified neuro-interventionalist may be considered in stroke patients who present within 6 hours
of onset (Class I, Level B recommendation). However, the availability of intra-arterial
thrombolysis should not preclude the administration of IV rtPA in eligible patients (Class III,
Level C evidence). Endovascular intervention, including angioplasty and disruption or removal
of the clot, is another option available at some specialized stroke centers for patients within 8
hours of last known well. Several devices have been approved by the FDA to recanalize occluded
vessels, but guideline recommendations for mechanical revascularization are generally lacking.
Urgent anticoagulation in acute ischemic stroke is no longer recommended and should not be
used to replace IV rtPA therapy in eligible patients (Class III, Level A evidence). Oral aspirin
therapy at a dose of 325 mg daily is recommended 24 to 48 hours after stroke onset in most
patients (Class I, Level A evidence), but it should not be given within 24 hours following rtPA
therapy (Class III, Level A and B).
In patients who are eligible for rtPA, treatment of arterial hypertension is recommended (Class I,
Level C evidence) with a goal blood pressure of less than 185/110 mm Hg before rTPA is
administered. Close post-lysis monitoring, with antihypertensive treatment given according to
the rtPA protocol, is also crucial to prevent hemorrhage (Class I, Level B evidence). In patients
who are not candidates for rtPA, blood pressure management in the acute setting is still
controversial, but the consensus is that antihypertensive medications should be withheld unless
systolic blood pressure is higher than 220 or diastolic blood pressure is higher than 120 (Class I,
Level C evidence). After 24 hours, initiation of antihypertensive agents is considered relatively
safe for patients with pre-existing hypertension.

Hypoxemia should be treated with supplemental oxygen, and fever should be treated with
antipyretic agents (Class I, Level C evidence). Euglycemia should be targeted, because persistent
hyperglycemia has been associated with poor outcomes (Class IIa, Level C evidence).
Patients should be admitted to specialized stroke care units incorporating rehabilitation when
possible (Class I, Level A evidence). Close monitoring during the first 72 to 96 hours of acute
ischemic stroke is important to assess for signs of hemorrhagic transformation or brain edema
(Class I, Level B evidence). Decompressive surgery in the setting of malignant edema may be
life-saving, but the morbidity is unknown in the setting of major cerebral hemispheric infarctions
(Class IIa, Level B evidence).
Treatment of concomitant medical illnesses, pneumonia, and urinary tract infections is
recommended (Class I, Level B and C evidence). Screening swallow evaluations should be
performed to assess the patient's risk for aspiration pneumonia (Class I, Level B evidence).
Subcutaneous anticoagulation or sequential compression devices should be instituted to prevent
formation of deep venous thrombosis, especially in patients with decreased mobility (Class I,
Level A evidence). Additional early and late complications are listed in Box 3.

Box 3: Early and Late Complications of Stroke

Early Complications (within 7 days)
Cerebral edema and herniation (within 96 hr)
Expansion of the infarct/recurrent infarction
Hemorrhagic transformation of the infarcted area
Seizure
Aspiration pneumonitis
Gastrointestinal ulcers and/or bleeding
Deep vein thrombosis and pulmonary embolism

Myocardial infarction
Late Complications (>7 days later)

Recurrent stroke
Seizure
Aspiration pneumonitis
Deep vein thrombosis and pulmonary embolism
Decubitus ulcer
Persistent cognitive or language dysfunction
Persistent loss of mobility

Spasticity

Primary Prevention
The American Heart Association and American Stroke Association issued a guideline for the
primary prevention of stroke in 2010 and one focused on the management of patients with
extracranial carotid stenoses in 2011, which are summarized here.

Each patient should undergo formal assessment of his or her stroke risk (Class I, Level A
evidence).
Hypertension has been well documented to increase the risk of stroke, and current
recommendations are to perform regular screening for hypertension a (Class I, Level A
evidence). Diet and lifestyle should be modified and pharmacologic treatment should be
prescribed according to the JNC 7 recommendations. Currently, guidelines emphasize
individualization of therapy, with the overall goal being blood pressure reduction to at
least less than 140/90 mm Hg.
In patients with diabetes, stricter blood pressure control to less than 130/80 mm Hg with
use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers is
recommended (Class I, Level A evidence). In these patients, a statin to lower the risk of
first stroke is also recommended (Class I, Level A evidence). Tight glycemic control is
encouraged to reduce microvascular complications, but evidence showing a reduction in
stroke risk is lacking.
In patients with dyslipidemia, recommendations state that those with known coronary
disease and patients at high-risk for coronary disease be treated with lifestyle measures
and a statin, even in the presence of a normal LDL (Class I, Level A evidence). In
patients with atrial fibrillation, warfarin therapy with a target international normalized
ratio of 2.0 to 3.0 is recommended in those without contraindications to oral
anticoagulants (Class I, Level A evidence).
Smoking doubles the risk of ischemic stroke and doubles or quadruples the risk of
subarachnoid hemorrhage. Smoking cessation is recommended (Class I, Level B
evidence) and the use of counseling, nicotine replacement, and oral medications should
be considered (Class IIa, Level B evidence). In addition, it is reasonable to avoid
exposure to environmental smoke (Class IIa, Level C evidence).
Physical activity is recommended to reduce the risk of stroke (Class I, Level B evidence).
Adults should engage in 2 hours and 30 minutes of moderate intensity activity each week
or one hour and 15 minutes of vigorous intensity aerobic activity each week (Class I,
Evidence B evidence).
Currently, aspirin therapy is not recommended for primary stroke prevention in people at
low risk for a cardiovascular event (Class III, Level A evidence), but it may be helpful in
primary stroke prevention for people whose risk is sufficiently high for the benefits to
outweigh the risks (a 10-year risk of cardiovascular events of 6% to 10%) (Class I, Level
A evidence).
In patients with asymptomatic carotid artery stenosis, screening for other treatable causes
of stroke and aggressive control of all risk factors is recommended (Class I, Level C
evidence). Aspirin therapy is recommended in the absence of contraindications (Class I,
Level A evidence). Selection of asymptomatic patients for carotid revascularization
should be guided by an assessment of multiple different factors and discussion of risk and
benefits of the procedure (Class I, Level C evidence). Prophylactic carotid
endarterectomy is reasonable in selected patients with high-grade asymptomatic carotid
stenosis if the risk of perioperative complications is low (Class IIa, Level A evidence).
Carotid artery angioplasty and stenting may be considered in asymptomatic patients, but
its effectiveness compared with medical therapy has not been well established (Class IIb,
Level B evidence). For both symptomatic and asymptomatic patients with high-grade
carotid stenosis who are at high risk of complications with revascularization, the

effectiveness of revascularization over medical management is also not established (Class

IIb, Level B evidence).
Secondary Prevention
Following a stroke, lifestyle changes should be made, with particular attention to reducing risk
factors for stroke as outlined earlier. In patients with atrial fibrillation, warfarin therapy is
recommended for preventing recurrent stroke in the absence of contraindications. In patients
with a history of noncardioembolic ischemic stroke, antiplatelet therapy is recommended.
Aspirin, clopidogrel, and dipyridamole in combination with low-dose aspirin have all been
shown to be beneficial in reducing the risk of recurrent stroke in multiple clinical trials. The most
recently published study, the PRoFESS trial from 2008, directly compared clopidogrel alone and
dipyridamole in combination with low-dose aspirin for preventing recurrent stroke. Although the
results did not meet the predefined statistical criteria for noninferiority, there was no statistically
significant difference between the groups in the primary outcome of recurrent stroke. However,
there was an increase in the rate of intracranial hemorrhage with the dipyridamole and aspirin
arm, which was not seen in prior studies evaluating this combination. Currently there is no clear
uniform recommendation of one agent over another, and therapy must be tailored to individual
patients based on availability, cost, and side-effect profile.
For patients with symptomatic high-grade carotid artery stenosis, carotid endarterectomy is
recommended for patients within 6 months of the stroke event if they are at average or low risk
(Class I, Level A evidence). Carotid stenting is an alternative to CEA for symptomatic patients at
average or low risk (Class I, Level B evidence) based upon the Carotid Revascularization
Endarterectomy versus Stenting Trial (CREST), which demonstrated no significant difference in
the primary outcome of stroke, death, or myocardial infarction, in symptomatic or asymptomatic
patients randomized to CEA or stenting.
Considerations in Special Populations
In patients with known medical conditions that increase the risk of stroke, such as sickle cell
disease, vasculitis, or cardiomyopathy, the approach to stroke prevention should be a coordinated
effort among the patient, the primary care physician, and involved specialists. Often, it is
important to aggressively manage the underlying disease state. The risk of ischemic stroke or
intracerebral hemorrhage is 2.4 times greater during pregnancy and the first 6 weeks following
delivery. Focal neurologic signs in this population merits prompt evaluation by a neurologist.
Other special considerations include children or young adults with stroke and patients in whom
no clear etiology of stroke is determined. Further workup may include referral to a geneticist for
evaluation of potential genetic or metabolic causes of stroke in these populations.
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Outcomes
During the hospitalization for an acute stroke, intensive speech, physical, and occupational
therapy should be initiated as soon as the patient is stable enough to participate. Most functional

recovery occurs within the first 3 months. After this, further recovery is possible, but it is
generally limited. The 1-year mortality in first-time stroke sufferers is 14% to 24% in persons
aged 40 to 69 years, and the 1-year mortality increases to 22% to 27% in patients aged 70 years
and older. Following a first stroke, the mean survival for persons aged 60 to 79 years ranges from
5.4 to 7.4 years. After age 80 years, the mean survival decreases to 1.8 years for men and 3.1
years for women.
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Summary

A stroke is defined as a sudden focal loss of neurologic function due to decreased

perfusion of brain tissue.
In patients who present with stroke symptoms, a rapid, focused neurologic history and
physical examination should be performed, making every attempt to establish a specific
time of onset because this helps to guide further therapy.
Patients presenting within a 4.5-hour time window of last known well should receive IV
rtPA at a dose of 0.9 mg/kg (maximum dose 90 mg) after a CT brain excludes the
presence of an intracranial hemorrhage and there are no other contraindications to
therapy. The dose is administered over 60 minutes, with 10% of the total dose being
given initially as a bolus.
The remaining hospital course is focused on evaluating potential etiologies of stroke,
preventing early complications, and performing intensive rehabilitation.
Anticoagulation should be considered for patients with a history of cardioembolic stroke,
and antiplatelet therapy should be considered for ischemic strokes of noncardiac etiology.
Optimization of stroke risk factor reduction is critical in both primary and secondary
prevention.

The recommendations on early management of adults with ischemic stroke and prevention are
based on guidelines from the American Heart Association and American Stroke Association.
Data regarding clinical trials in ischemic stroke are available at strokecenter.org.
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Suggested Readings

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