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 third-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 Modifiable Not Modifiable

Hypertension
Age >55
Diabetes
Male gender
Atrial fibrillation
Ischemic stroke Black race
Smoking
Family history of stroke
Hyperlipidemia
Personal history of stroke
Carotid stenosis
Hypertension Vascular malformation
Amyloid angiopathy Neoplasm
Intraparenchymal hemorrhage
Anticoagulant use Trauma
Thrombolytic use Acute ischemic stroke
Aneurysm
Family history of aneurysm or connective tissue disease
Subarachnoid hemorrhage
Other vascular malformation
Trauma

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Pathophysiology and natural history

Ischemic Stroke

Based on prior clinical trials, a subclassification scheme of five categories of ischemic stroke has become
widely accepted. These categories are based on etiology and are as follows: 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 extracranial 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 often leads 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.

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 brainstem.

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.

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 and hemorrhage 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
and occur 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 benign.

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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 Area Affected Signs and Symptoms

Frontal pole and mesial Contralateral: leg > face and arm weakness
Anterior cerebral artery
frontal lobe Frontal signs such as abulia
Contralateral: face and arm > leg weakness, sensory loss
to all modalities, visual field cut, visual-spatial neglect
Posterior frontal, temporal,
Middle cerebral artery Ipsilateral: gaze preference
parietal lobes
Dominant hemisphere affected: aphasia, alexia, agraphia,
acalculia
Contralateral: homonymous hemianopia
Posterior cerebral
Occipital lobe With thalamic involvement: Sensory loss to all modalities
artery
or pain
Contralateral: hemiparesis and hemisensory loss of pain
Anterior inferior
Lateral pontine syndrome and temperature
cerebellar artery
Ipsilateral: ataxia
Contralateral: hemibody pain and temperature loss
Ipsilateral: facial pain, hemifacial pain and temperature
Posterior inferior Lateral medulla (Wallenberg
loss, ataxia, nystagmus, nausea/vomiting, vertigo,
cerbellar artery syndrome)
Horner's syndrome, dysphagia
Hiccups
Bilateral: progressive quadriplegia, facial weakness
Basilar artery Pons (locked-in syndrome)
Lateral gaze weakness with sparing of vertical gaze
Contralateral: hemibody weakness, loss of vibration
Vertebral artery Medial medulla and proprioception
Ipsilateral: tongue weakness and/or atrophy
Vertebral artery Lateral medulla 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, onset is determined at 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).

Laboratory Tests

In patients presenting with sudden onset of focal neurologic deficit, baseline laboratory testing should be
performed. This consists of point-of-care blood glucose testing, basic metabolic panel, complete blood count,
cardiac enzymes, and coagulation studies (Class I, Level B recommendation). A 12-lead electrocardiogram
(ECG) should be performed in all stroke patients (Class I, Level B recommendation). If subarachnoid
hemorrhage is suspected, cerebrospinal fluid should be obtained and sent for differential red blood cell counts in
serial tubes.

Once the patient is stabilized, further testing such as lipid panel and hemoglobin A1C studies should be sent to
assist in identifying risk factors. If no clear etiology is identified, further laboratory testing to assess for a
hypercoagulable state, genetic or metabolic disturbance, or inflammatory conditions should be performed.

Imaging
With advances in technology, imaging has become integral in the evaluation and management of acute stroke
patients. In all patients who present to the hospital with a suspected stroke, the first imaging study should be an
emergent noncontrast computed tomography (CT) scan of the brain to assess for intracranial hemorrhage. CT
angiography with and without perfusion studies rapidly provides visualization of blood flow and is used in the
acute setting at some tertiary stroke centers to identify the location of vascular occlusion and assess for
salvageable brain tissue (Class I, Level A recommendation). However, because the study uses contrast, renal
function should ideally be known and documented before proceeding. Cerebral angiography may also be
undertaken emergently, particularly in cases when vascular intervention is being considered.

In the last several years, MRI has emerged as an invaluable tool in the care of stroke patients. A specialized
MRI sequence that measures the diffusion of water, known as diffusion-weighted imaging (DWI), allows
visualization of acute strokes that range in age from a few hours to 1 week. This is especially helpful in stroke
patients who present within 24 to 48 hours of symptom onset because an acute ischemic lesion can often be
missed on a routine CT scan early on. MR angiography is also a useful method for evaluating intra- and
extracranial vasculature, although the degree of stenosis in diseased vessels is often overestimated by this
technique. Other studies that assess cerebral blood flow include carotid ultrasound and transcranial Doppler
ultrasonagraphy (TCD), which are noninvasive tests that use pulsatility indices and mean flow velocities to
evaluate the vasculature.

Other Diagnostic Tests

All patients with ischemic stroke should have a transthoracic echocardiogram (TTE) to assess for a
cardioembolic source, which includes left ventricular or valvular dysfunction, intracardiac thrombus, and patent
foramen ovale. In patients who are strongly suspected to have a cardioembolic stroke despite a negative TTE,
further testing with transesophageal echocardiogram or TCD with breath-holding should be performed as these
studies increase the detection of an intra-cardiac shunt. Duplex ultrasonography of the legs should also be
considered in patients in whom a paradoxical embolus is suspected.

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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 (EMS) 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 onset and have no evidence of hemorrhage or
infarct size greater than one third of the middle cerebral artery territory on CT brain, 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 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. Box
2 lists conditions excluding patients from t-PA therapy.

Box 2: Exclusion Criteria for Treatment of Acute Ischemic Stroke with rtPA
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

CT, computed tomography; INR, international normalized ratio; PTT, partial thromboplastin time; rtPA,
recombinant tissue plasminogen activator.

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.

Although used previously, urgent anticoagulation in acute ischemic stroke is not 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 72 hr)
• Expansion of the infarct/recurrent infarction
• Hemorrhagic transformation of the infracted area
• Seizure
• Aspiration pneumonitis
• Gastrointestinal ulcers and/or bleeding
• Deep vein thrombosis and thromboembolism

• Myocardial infarction
Late Complications (>7 days later)
• Recurrent stroke
• Seizure
• Aspiration pneumonitis
• Deep vein thrombosis and thromboembolism
• Persistent cognitive or language dysfunction
• Persistent loss of mobility

• Spasticity

Primary Prevention

In 2006, the American Heart Association and American Stroke Association issued a guideline for the primary
prevention of ischemic stroke, which is summarized here.

• Each patient should undergo formal assessment of his or her stroke risk (Class I, Level A evidence).
• Those with coronary artery disease, heart failure, or symptomatic peripheral arterial disease are 1.73
times more likely to have a first stroke as compared to those without these conditions. Antiplatelet
therapy is recommended in these patients.
• Hypertension has been well documented to increase the risk of stroke, and current recommendations are
to perform screening for hypertension at least every 2 years in adults (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 (ACE) inhibitors or angiotensin receptor blockers (ARBs) 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 high-
risk hypertensive patients 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 (INR) of 2.0 to 3.0 is recommended in those without
contraindications to oral anticoagulants (Class I, Level of A evidence).
• Smoking doubles the risk of ischemic stroke and doubles or quadruples the risk of hemorrhagic stroke.
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).
• Currently, aspirin therapy is not recommended for primary stroke prevention in men (Class III, Level A
evidence), but it may be helpful in primary stroke prevention among women older than 65 years who
have well-controlled hypertension (Class IIa, Level B evidence).
• Carotid endarterectomy is recommended for patients with symptomatic high-grade carotid artery
stenosis because surgery was shown to be beneficial in significantly reducing stroke risk (9%) at 2 years
versus medical therapy with aspirin alone (26%). In patients with asymptomatic carotid artery stenosis,
screening for other treatable causes of stroke with 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 of B evidence). Prophylactic carotid endarterectomy is recommended in selected patients with
high-grade asymptomatic carotid stenosis; endarterectomy should be performed by surgeons with less
than 3% morbidity and mortality postoperative complication rates (Class I, Level of A evidence).
Carotid artery angioplasty and stenting may be considered in asymptomatic patients who are at high
surgical risk for endarterectomy (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.

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.

Temporary stroke symptoms due to ischemia that last less than 24 hours are typically referred to as a transient
ischemic attack (TIA). After a TIA, the 90-day risk of stroke is 3% to 17.3%, and the risk is highest within the
first 30 days. Within a year of a TIA, up to 25% of patients die.

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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 3-hour time window of symptom onset 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 www.strokecenter.org.

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References