Ischemic Stroke Deep tendon reflexes

Practice Essentials Mental status

Stroke is characterized by the sudden loss of blood level of consciousness
circulation to an area of the brain, resulting in a The patients skull and spine also should be examined, and
corresponding loss of neurologic function. Strokes are signs of meningismus should be sought.
classified as either hemorrhagic or ischemic. Acute ischemic Laboratory studies
stroke refers to stroke caused by thrombosis or embolism Laboratory tests performed in the diagnosis and evaluation
and is more common than hemorrhagic stroke. of ischemic stroke include the following:
Essential update: Thrombolysis within 90 minutes yields Complete blood cell count: The CBC count serves as a
excellent results in patients with mild to moderate baseline study and may reveal a cause for the stroke (eg,
ischemic stroke polycythemia, thrombocytosis, thrombocytopenia, leukemia)
Administration of intravenous recombinant tissue-type or provide evidence of concurrent illness (eg, anemia)
plasminogen activator (rt-PA) is most effective within 90 Basic chemistry panel: The chemistry panel serves as a
minutes of the onset of stroke symptoms, according to a 10- baseline study and may reveal a stroke mimic (eg,
center European study of nearly 6900 patients. The hypoglycemia, hyponatremia) or provide evidence of
investigators found that patients who scored in the 7-12 concurrent illness (eg, diabetes, renal insufficiency)
range on the National Institutes of Health Stroke Scale Coagulation studies: Coagulation studies may reveal a
(NIHSS) had better outcomes when thrombolytic therapy coagulopathy and are useful when thrombolytics or
was provided within the first hour and a half of symptom anticoagulants are to be used
onset than did those treated between 90 and 270 minutes Cardiac biomarkers: Cardiac biomarkers are important
after onset, with the earlier-treated patients demonstrating because of the association of cerebral vascular disease and
little or no disability 3 months after thrombolysis. For coronary artery disease
patients with minor stroke or moderate to severe stroke, Toxicology screening: Toxicology screening may assist in
however, treatment within the 90-minute window provided no identifying intoxicated patients with symptoms/behavior
additional advantage.[1, 2] mimicking stroke syndromes
Signs and symptoms Pregnancy testing: A urine pregnancy test should be
obtained for all women of childbearing age with stroke
Although signs and symptoms of stroke can occur alone, they
symptoms; recombinant tissue-type plasminogen activator
are more likely to occur in combination. Common stroke signs
(rt-PA) is a pregnancy class C agent
and symptoms include the following:
Arterial blood gas analysis: Although infrequent in patients
Abrupt onset of hemiparesis, monoparesis, or quadriparesis
with suspected hypoxemia, arterial blood gas defines the
Acute hemisensory loss
severity of hypoxemia and may be used to detect acid-base
Complete or partial hemianopia, monocular or binocular
disturbances
visual loss, or diplopia
Imaging studies
Visual field deficits
Imaging in ischemic stroke can involve the following
Diplopia
modalities:
Dysarthria
Several types of magnetic resonance imaging
Ataxia
Several types of computed tomography scanning
Vertigo
Angiography
Nystagmus
Ultrasonography
Aphasia
Radiology
Sudden decrease in the level of consciousness
Echocardiography
In younger patients, a history of recent trauma,
Nuclear imaging
coagulopathies, illicit drug use (especially cocaine), migraines,
Lumbar puncture
or use of oral contraceptives should be elicited.
A lumbar puncture is required to rule out meningitis or
See Clinical Presentation for more detail.
subarachnoid hemorrhage when the CT scan is negative but
Diagnosis
the clinical suspicion remains high
With the availability of thrombolytic therapy for acute See Workup for more detail.
ischemic stroke in selected patients, the physician must be Management
able to perform a brief, but accurate, neurologic examination
Ischemic stroke therapies include the following:
on patients with suspected stroke syndromes. Essential
Thrombolytic therapy: Thrombolytics restore cerebral
components of the neurologic examination include evaluations
blood flow among some patients with acute ischemic stroke
of the following:
and may lead to improvement or resolution of neurologic
Cranial nerves
deficits
Motor function
Antiplatelet agents: The International Stroke Trial and the
Sensory function
Chinese Acute Stroke Trial (CAST) demonstrated modest
Cerebellar function
benefit from the use of aspirin in the setting of acute
Gait
ischemic stroke[3, 4]
 Mechanical thrombolysis: Involves the endovascular
treatment of acute ischemic stroke
Stroke prevention
Primary stroke prevention refers to the treatment of
individuals with no previous history of stroke. Measures may
include use of the following:
Platelet antiaggregants
3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)
reductase inhibitors (ie, statins)
Exercise
Secondary prevention refers to the treatment of individuals
who have already had a stroke. Measures may include use of
the following:
Platelet antiaggregants
Antihypertensives
HMG-CoA reductase inhibitors (statins)
Lifestyle interventions
See Treatment and Medication for more detail.
Image library
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.
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.[5] )
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[6] :
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.[7] The trials 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.[8] 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.[9] 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) 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).
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. See
the Cardiac Output calculator.
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 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 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 Structures Supplied
TERRITORY
Anterior Circulation
(Carotid)
Anterior Cerebral Cortical branches: medial frontal and
Artery parietal lobe
Medial lenticulostriate
 temporal lobes. The anterior choroidal artery (yellow)
branches: caudate head, globus
supplies the posterior limb of the internal capsule and part of
pallidus, anterior limb of internal
the hippocampus extending to the anterior and superior
capsule
surface of the occipital horn of the lateral ventricle.

Middle Cerebral Cortical branches: lateral frontal

Artery and parietal lobes lateral and anterior
temporal lobe

Lateral lenticulostriate
branches: globus pallidus and
putamen, internal capsule
Vascular distributions: MCA
infarction. Noncontrast CT demonstrates a large acute
infarction in the MCA territory involving the lateral surfaces
Anterior Choroidal Optic tracts, medial temporal lobe, of the left frontal, parietal, and temporal lobes, as well as
Artery ventrolateral thalamus, corona the left insular and subinsular regions, with mass effect and
radiata, posterior limb of the internal rightward midline shift. There is sparing of the caudate head
capsule and at least part of the lentiform nucleus and internal
capsule, which receive blood supply from the lateral
Posterior Circulation
lenticulostriate branches of the M1 segment of the MCA.
(Vertebrobasilar)
Note the lack of involvement of the medial frontal lobe (ACA
Posterior Cerebral Cortical branches: occipital lobes, territory), thalami and paramedian occipital lobe (PCA
Artery medial and posterior temporal and
parietal lobes

Perforating branches: brainstem, territory). Vascular

posterior thalamus and midbrain 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
Posterior Inferior Inferior vermis; posterior and diffusion in a larger ACA infarction involving the left
Cerebellar Artery inferior cerebellar hemispheres paramedian frontal and posterior parietal regions. There is
also infarction of the lateral temporoparietal regions
Anterior Inferior Anterolateral cerebellum bilaterally (both MCA distributions), greater on the left
Cerebellar Artery indicating multivessel involvement suggesting emboli.
Superior Cerebellar Superior vermis; superior cerebellum
Artery

Vascular distributions:
PCA infarction. The noncontrast CT images demonstrate PCA
distribution infarction involving the right occipital and
The supratentorial inferomedial temporal lobes. The image on the right
vascular territories of the major cerebral arteries are demonstrates additional involvement of the thalamus, also
demonstrated superimposed on axial (left) and coronal (right) part of the PCA territory.
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

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.
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.[10, 11, 12]
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.[13]
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
barriers 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.[14, 15]
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.[13] 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 fluidlike 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
[10, 16, 17]
intraparenchymal hematoma.
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.[10, 18, 7]Hemorrhagic
transformation is also more likely following administration of
t-PA, with noncontrast computed tomography (NCCT)
scanning demonstrating areas of hypodensity.[19, 20, 21]
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%).[22] 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.[22] A fraction of patients who have experienced
stroke develop chronic seizure disorders.
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
In a prospective study of 27,860 women aged 45 years or
older who were participating in the Women's Health Study,
Kurth et al found that migraine with aura was a strong risk
factor for any type of stroke.[23] The adjusted incidence of
this risk factor per 1000 women per year was similar to those
of other known risk factors, including systolic blood pressure
180 mm Hg or higher, body mass index 35 kg/m2 or greater,
history of diabetes, family history of myocardial infarction,
and smoking.[23]
For migraine with aura, the total incidence of stroke in the
study was 4.3 per 1000 women per year, the incidence of
ischemic stroke was 3.4 per 1000 per year, and the incidence
of hemorrhagic stroke was 0.8 per 1000 per year.
Modifiable risk factors for ischemic stroke 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.[24]
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.[25, 26]
Antipsychotic medications
An analysis of 14,584 stroke patients who had at least 1
antipsychotic prescription during the year before their first
hospitalization for stroke indicated that in the first few
weeks of use, antipsychotics are associated with an increased
stroke risk. Dosage size, older age and/or the presence of
dementia, and the use of antipsychotics with a high binding
affinity for alpha-2-adrenergic and M1-muscarinic receptors
contributed to the stroke risk.[27]
According to the investigators, the stroke risk in persons
taking antipsychotic medications was 1.6-fold higher in the 2
weeks before the stroke occurred. However, this association
was observed only in the initial 28 days of antipsychotic use,
after which the drugs were no longer a contributing factor in
stroke.
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:
Metabolic Disease and Stroke - Methylmalonic Acidemia
Metabolic Disease and Stroke -
Homocystinuria/Homocysteinemia
Metabolic Disease and Stroke - Fabry Disease
Metabolic Disease and Stroke MELAS
Metabolic Disease and Stroke -
Hyperglycemia/Hypoglycemia
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.)
 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
Noncontrast CT in this 52-
can occur in the deep gray matter structures, corona radiata,
year-old male with a history of worsening right-sided
brainstem and cerebellum.
weakness and aphasia demonstrates diffuse hypodensity and
Causes of lacunar infarcts include the following:
sulcal effacement involving the left anterior and middle
cerebral artery territories consistent with acute infarction.
Microatheroma
There are scattered curvilinear areas of hyperdensity noted
Lipohyalinosis
suggestive of developing petechial hemorrhage in this large 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.
area of infarction. MRA in
Emboli may arise from the heart, the extracranial arteries,
the same patient as in the above image (left) demonstrates
or, rarely, the right-sided circulation (paradoxical emboli)
occlusion of the left precavernous supraclinoid internal
with subsequent passage through a patent foramen ovale. The
carotid artery (ICA, red circle), occlusion or high-grade
sources of cardiogenic emboli include the following:
stenosis of the distal MCA trunk and attenuation of multiple
M2 branches. The diffusion-weighted image (right)
Valvular thrombi (eg, in mitral stenosis or endocarditis or
from use of a prosthetic valve)
demonstrates high signal confirmed to be true restricted
diffusion on the ADC map consistent with acute infarction.
Mural thrombi (eg, in myocardial infarction [MI], atrial
fibrillation [AF], dilated cardiomyopathy, or severe
congestive heart failure [CHF])
Atrial myxoma
MI is associated with a 2-3% incidence of embolic strokes, of
which 85% occur in the first month after MI.[28] 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
MIP image from a CTA
specific for cardioembolism. Multiple and bilateral infarcts
demonstrates a filling defect or high-grade stenosis at the
can be the result of embolic showers or recurrent emboli.
branching point of the right MCA trunk (red circle),
Other possibilities for single and bilateral hemispheric
suspicious for thrombus or embolus. CTA is highly accurate in
infarctions include emboli originating from the aortic arch
detecting large vessel stenosis and occlusions, which account
and diffuse thrombotic or inflammatory processes that can
for approximately one third of ischemic strokes.
lead to multiple small-vessel occlusions.[29, 30] (See the image
Lacunar strokes
below.)
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.)
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.
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[31, 10] :
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.[32, 33, 34]
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.
Epidemiology
Stroke is the leading cause of disability and the third leading
cause of death in the United States.[35]
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.[36]
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.[37]
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.[36] Risk of stroke increases with age, especially in
patients older than 64 years, in whom 75% of all strokes
occur.
Prognosis
The prognosis after acute ischemic stroke varies greatly,
depending on the stroke severity and on the patients
premorbid condition, age, and poststroke complications.[6]
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.[7, 38, 39]
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.[40, 41, 42]
To see complete information on Motor Recovery in Stroke,
please go to the main article by clicking here.
 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
History
A focused medical history for patients with ischemic stroke
aims to identify risk factors for atherosclerotic and cardiac
disease, including hypertension, diabetes mellitus, tobacco
use, high cholesterol, and a history of coronary artery
disease, coronary artery bypass, or atrial fibrillation (see
Etiology). Consider stroke in any patient presenting with
acute neurologic deficit or any alteration in level of
consciousness. Common signs of stroke include the following:
Acute hemiparesis or hemiplegia
Acute hemisensory loss
Complete or partial hemianopia, monocular or binocular
visual loss, or diplopia
Dysarthria or aphasia
Ataxia, vertigo, or nystagmus
Sudden decrease in consciousness
In younger patients, elicit a history of recent trauma,
coagulopathies, illicit drug use (especially cocaine), migraines,
or use of oral contraceptives.
Establishing the time at which the patient was last without
stroke symptoms is especially critical when thrombolytic
therapy is an option. If the patient awakens with symptoms,
then the time of onset is defined as the time at which the
patient was last seen to be without symptoms. Family
members, coworkers, and bystanders may be required to help
establish the exact time of onset, especially in right
hemispheric strokes accompanied by neglect or left
hemispheric strokes with aphasia.
Physical Examination
The goals of the physical examination include detecting
extracranial causes of stroke symptoms, distinguishing
stroke from stroke mimics, determining and documenting for
future comparison the degree of deficit, and localizing the
lesion.
The physical examination always includes a careful head and
neck examination for signs of trauma, infection, and
meningeal irritation.
Stroke should be considered in any patient presenting with an
acute neurologic deficit (focal or global) or altered level of
consciousness. No historical feature distinguishes ischemic
from hemorrhagic stroke, although nausea, vomiting,
headache, and change in level of consciousness are more
common in hemorrhagic strokes.
Common symptoms of stroke include the following:
Abrupt onset of hemiparesis, monoparesis, or quadriparesis
Hemisensory deficits
Monocular or binocular visual loss
Visual field deficits
Diplopia
Dysarthria
Ataxia
Vertigo
Aphasia
Sudden decrease in the level of consciousness
Although such symptoms can occur alone, they are more likely
to occur in combination.
A careful search for the cardiovascular causes of stroke
requires examination of the ocular fundi (retinopathy, emboli,
hemorrhage), heart (irregular rhythm, murmur, gallop), and
peripheral vasculature (palpation of carotid, radial, and
femoral pulses, auscultation for carotid bruit).
Patients with a decreased level of consciousness should be
assessed to ensure that they are able to protect their
airway.
The physical examination must encompass all of the major
organ systems, starting with the airway, breathing, and
circulation (ABC) and the vital signs. Patients with stroke,
especially hemorrhagic stroke, can clinically deteriorate
quickly; therefore, constant reassessment is critical.
Ischemic strokes, unless large or involving the brainstem, do
not tend to cause immediate problems with airway patency,
breathing, or circulation compromise. On the other hand,
patients with intracerebral or subarachnoid hemorrhage
frequently require intervention for airway protection and
ventilation.
Vital signs, while nonspecific, can point to impending clinical
deterioration and may assist in narrowing the differential
diagnosis. Many patients with stroke are hypertensive at
baseline, and their blood pressure may become more elevated
after stroke. While hypertension at presentation is common,
blood pressure decreases spontaneously over time in most
patients. Acutely lowering blood pressure has not proven to
be beneficial in these stroke patients in the absence of signs
and symptoms of associated malignant hypertension, acute
myocardial infarction, CHF, or aortic dissection.
Head and neck examination
A careful examination of the head and neck is essential.
Contusions, lacerations, and deformities may suggest trauma
as the etiology for the patient's symptoms. Auscultation of
the neck may elicit a bruit, suggesting carotid disease as the
cause of the stroke.
Cardiac examination
Cardiac arrhythmias, such as atrial fibrillation, are found
commonly in patients with stroke. Similarly, strokes may
occur concurrently with other acute cardiac conditions, such
 as acute myocardial infarction and acute CHF; thus, Table 2. NIH Stroke Scale (Open Table in a new window)
auscultation for murmurs and gallops is recommended.
Category Description Score
Examination of the extremities
Carotid or vertebrobasilar dissections and, less commonly, 1a level of consciousness (LOC) Alert 0
thoracic aortic dissections may cause ischemic stroke.
Unequal pulses or blood pressures in the extremities may
reflect the presence of aortic dissections.
Neurologic examination Drowsy 1
With the availability of thrombolytic therapy for acute
ischemic stroke in selected patients, the physician must be
able to perform a brief, but accurate, neurologic examination
on patients with suspected stroke syndromes. The goals of Stuporous 2
the neurologic examination include the following:
Confirming the presence of a stroke syndrome (to be
defined further by cranial computed tomography [CT]
scanning) Coma 3
Distinguishing stroke from stroke mimics
Establishing a neurologic baseline should the patient's
condition improve or deteriorate 1b LOC questions (month, age) Answers both 0
Essential components of the neurologic examination include correctly
the evaluation of cranial nerves, motor function, sensory
function, cerebellar function, gait, and deep tendon reflexes,
as well as of mental status and level of consciousness. The 1
skull and spine also should be examined, and signs of Answers 1
meningismus should be sought. correctly
Central facial weakness from a stroke should be
differentiated from the peripheral weakness of Bell palsy. 2
With peripheral lesions (Bell palsy), the patient is unable to
lift the eyebrows, wrinkle the forehead, or or close the eye Incorrect on
on the affected side. both
A useful tool in quantifying neurological impairment is the
National Institutes of Health Stroke Scale (NIHSS). The
NIHSS (see Table 2, below and the NIH Stroke
Score calculator) is used mostly by stroke teams. It enables 1c Answers both correctly Obeys both 0
the consultant to rapidly determine the severity and possible Answers 1 correctly Incorrect correctly
location of the stroke. A patient's score on the NIHSS is on both
strongly associated with outcome, and it can help to identify
those patients who are likely to benefit from thrombolytic 1
therapy and those who are at higher risk of developing Obeys 1
hemorrhagic complications of thrombolytic use. correctly
This scale is easily used and focuses on the following 6 major
areas of the neurologic examination: 2
level of consciousness
Visual function Incorrect on
Motor function both
Sensation and neglect
Cerebellar function
Language
The NIHSS is a 42-point scale, with minor strokes usually 2 Best gaze (follow finger) Normal 0
being considered to have a score less than 5. An NIHSS
score greater than 10 correlates with an 80% likelihood of
visual flow deficits on angiography. However, discretion must
be used in assessing the magnitude of the clinical deficit; for Partial gaze 1
instance, if a patient's only deficit is being mute, the NIHSS palsy
score will be 3. Additionally, the scale does not measure some
deficits associated with posterior circulation strokes (ie,
vertigo, ataxia).[43] 2
 Forced No movement
deviation

6 Motor arm right* (raise 90, No drift 0

3 Best visual (visual fields) No visual loss 0 hold 10 seconds)

Drift 1
Partial 1
hemianopia

Cannot resist 2
2 gravity
Complete
hemianopia
3
3 No effort
against gravity
Bilateral
hemianopia 4

No movement

4 Facial palsy (show teeth, raise Normal Minor 0

brows, squeeze eyes shut)
7 Motor leg left* (raise 30, No drift 0
hold 5 seconds)
Partial 1
Complete
Drift 1

Cannot resist 2
gravity
3

3
No effort
5 Motor arm left* (raise 90, No drift 0 against gravity
hold 10 seconds)
4

Drift 1 No movement

Cannot resist 2 8 Motor leg right* (raise 30, No drift 0

gravity hold 5 seconds)

3 Drift 1
No effort
against gravity

4 Cannot resist 2
gravity
 dysarthria
2
3
No effort
against gravity Near to
unintelligible or
4 worse

No movement

13 Best language** (name items, No aphasia 0

describe pictures)
9 Limb ataxia (finger-nose, heel- Absent 0
shin)
Mild to 1
moderate
Present in 1 1 aphasia
limb
2

2 Severe aphasia
Present in 2
limbs 3

Mute

10 Sensory (pinprick to face, Normal 0

arm, leg)
Total - 0-42

Partial loss 1 * For limbs with amputation, joint fusion, etc, score 9 and
explain.

Severe loss 2
** For intubation or other physical barriers to speech, score
9 and explain. Do not add 9 to the total score. NIH Stroke
Scale (PDF)
11 Extinction/neglect (double No neglect 0
simultaneous testing)

Middle cerebral artery stroke

Partial neglect 1 MCA occlusion commonly produces contralateral hemiparesis,
contralateral hypesthesia, ipsilateral hemianopsia, and gaze
preference toward the side of the lesion. Agnosia is common,
and receptive or expressive aphasia may result if the lesion
Complete 2 occurs in the dominant hemisphere. Neglect, inattention, and
neglect extinction of double simultaneous stimulation may occur in
nondominant hemisphere lesions. Since the MCA supplies the
upper extremity motor strip, weakness of the arm and face is
usually worse than that of the lower limb.
12 Dysarthria (speech clarity to Normal 0 Anterior cerebral artery stroke
"mama, baseball, huckleberry, articulation
ACA occlusions primarily affect frontal lobe function and can
tip-top, fifty-fifty")
result in disinhibition and speech perseveration, producing
primitive reflexes (eg, grasping, sucking reflexes), altered
1
mental status, impaired judgment, contralateral weakness
Mild to
(greater in legs than arms), contralateral cortical sensory
moderate
deficits gait apraxia, and urinary incontinence.
 Posterior cerebral artery stroke
PCA occlusions affect vision and thought, producing
contralateral homonymous hemianopsia, cortical blindness,
visual agnosia, altered mental status, and impaired memory.
Vertebrobasilar artery occlusions are notoriously difficult to
detect because they cause a wide variety of cranial nerve,
cerebellar, and brainstem deficits. These include the
following:
Vertigo
Nystagmus
Diplopia
Visual field deficits
Dysphagia
Dysarthria
Facial hypesthesia
Syncope
Ataxia
A hallmark of posterior circulation stroke is that there are
crossed findings: ipsilateral cranial nerve deficits and
contralateral motor deficits. This is contrasted to anterior
stroke, which produces only unilateral findings.
Lacunar stroke
Lacunar strokes result from occlusion of the small,
perforating arteries of the deep subcortical areas of the
brain. The infarcts are generally from 2-20 mm in diameter.
The most common lacunar syndromes include pure motor, pure
sensory, and ataxic hemiparetic strokes. By virtue of their
small size and well-defined subcortical location, lacunar
infarcts do not lead to impairments in cognition, memory,
speech, or level of consciousness.
Diagnostic Considerations
Stroke mimics commonly confound the clinical diagnosis of
stroke. One study reported that 19% of patients diagnosed
with acute ischemic stroke by neurologists before cranial CT
scanning actually had noncerebrovascular causes for their
symptoms.
The most frequent stroke mimics include the following:
Seizure (17%)
Systemic infection (17%)
Brain tumor (15%)
Toxic-metabolic cause, such as hyponatremia and
hypoglycemia (13%)
Positional vertigo (6%).
A critical masquerading metabolic derangement not to be
missed by providers is hypoglycemia.[44, 45]
For more information, see Metabolic Disease and Stroke
Hyperglycemia/Hypoglycemia.
Diagnosis and management of a rare form of stroke, cerebral
venous thrombosis (CVT), was the subject of a 2011
AHA/ASA statement for healthcare professionals. According
to the statement, diagnosing CVT requires a high degree of
clinical suspicion. Most people diagnosed with CVT present
with headache, often of increasing severity, usually but not
always accompanied by focal neurological signs.[46]
Differential Diagnoses
Acute Coronary Syndrome
Atrial Fibrillation
Bell Palsy
Benign Positional Vertigo
Brain Abscess
Epidural Hematoma
Hemorrhagic Stroke in Emergency Medicine
Inner Ear Labyrinthitis
Myocardial Infarction
Neoplasms, Brain
Subarachnoid Hemorrhage
Syncope
Transient Ischemic Attack
Approach Considerations
Laboratory evaluation of the patient with ischemic
stroke should be driven by comorbid illnesses as well
as the potential acute stroke. Additional laboratory
tests are tailored to the individual patient. They may
include rapid plasma reagent (RPR), toxicology
screen, fasting lipid profile, sedimentation rate,
pregnancy test, antinuclear antibody (ANA),
rheumatoid factor, and homocysteine.
CT is the most commonly used form of neuroimaging
in the acute evaluation of patients with apparent
acute stroke. MRI with magnetic resonance
angiography (MRA) has been a major advance in the
neuroimaging of stroke; MRI not only provides great
structural detail but also can demonstrate impaired
metabolism.
Carotid duplex scanning is one of the most useful
tests in evaluating patients with stroke.
Increasingly, it is being performed earlier in the
evaluation, not only to define the cause of the stroke
but also to stratify patients for either medical
management or carotid intervention if they have
carotid stenoses.
Digital subtraction angiography is considered the
definitive method for demonstrating vascular
lesions, including occlusions, stenoses, dissections,
and aneurysms.
Complete Blood Cell Count
CBC count serves as a baseline study and may reveal
a cause for the stroke (eg, polycythemia,
thrombocytosis, thrombocytopenia, leukemia) or
provide evidence of concurrent illness (eg, anemia).
Basic Chemistry Panel
Chemistry panel serves as a baseline study and may
reveal a stroke mimic (eg, hypoglycemia,
hyponatremia) or provide evidence of concurrent
illness (eg, diabetes, renal insufficiency).
Coagulation Studies
Coagulation studies may reveal a coagulopathy and
are useful when thrombolytics or anticoagulants are
to be used. In patients who are not anticoagulated
and in whom there is no suspicion for coagulation
abnormality, administration of recombinant tissue-
type plasminogen activator (rt-PA) should not be
delayed awaiting laboratory studies.
Cardiac Biomarkers
 Cardiac biomarkers are important because of the
association of cerebral vascular disease and coronary
artery disease. Additionally, several studies have
indicated a link between elevations of cardiac
enzyme levels and poor outcome in ischemic stroke.
Toxicology Screening
Toxicology screening may be useful in selected
patients in order to assist in identifying intoxicated
patients with symptoms/behavior mimicking stroke
syndromes. Urine pregnancy test should be obtained
for all women of childbearing age with stroke
symptoms. The agent rt-PA is Pregnancy Class C.
Arterial Blood Gas Analysis
Although infrequent in patients with suspected
hypoxemia, arterial blood gas defines the severity of
hypoxemia and may detect acid-base disturbances.
If considering thrombolytics, arterial punctures
should be avoided unless absolutely necessary.
Imaging in Stroke
Imaging in ischemic stroke can involve several types
of MRI, several types of CT scanning, angiography,
ultrasonography, radiology, echocardiography, and
nuclear imaging studies.
Magnetic resonance imaging
Conventional MRI may take hours to produce
discernable findings, well after the diffusion-
weighted images have become positive. For this
reason, many centers always include diffusion-
weighted images in their standard brain MRI
protocol. Diffusion-weighted MRI can detect
ischemia much earlier than can standard CT scanning
or MRI and provides useful data in stroke and TIA
patients outside of the initial management window.[22,
47, 48]
The most commonly used technique for
perfusion MRI is dynamic susceptibility, which
involves generating maps of brain perfusion by
monitoring the first pass of a rapid bolus injection
of contrast through the cerebral vasculature.
Susceptibility-related T2 effects create signal loss
in capillary blood vessels and parenchyma perfused
by contrast that can be measured and is proportional
to the CBV. (See the image below.)
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.
An evidence-based guideline from the American
Academy of Neurology recommends that diffusion-
weighted imaging (DWI) is more useful than
noncontrast CT for the diagnosis of acute ischemic
stroke within 12 hours of symptom onset and should
be performed for the most accurate diagnosis of
acute ischemic stroke (level A). No recommendations
were made regarding the use of perfusion-weighted
imaging (PWI) in diagnosing acute ischemic stroke, as
evidence to support or refute its value in this
setting is insufficient.[49]
A study by Bhattacharya et al concluded that the
early use of MRI helps to prevent emergency
departments from misdiagnosing ischemic stroke in
young adults presenting with signs of stroke.
Reviewing a prospective database of patients aged
16-49 years with ischemic stroke, the investigators
found that the chance of misdiagnosis was lower in
patients who had undergone MRI within 48 hours.[50]
The study also found that, in general, there is a
particular risk that emergency departments will
misdiagnose ischemic stroke in patients younger than
35 years, indicating that early MRI studies would be
especially beneficial in young adults with signs of
stroke.
Intra-arterial contrast enhancement may be seen
secondary to slow flow during the first or second
day after onset of infarction and has been
correlated with increased infarct volume size.[51]
The 3 different techniques used to produce MRA
images are 3-dimensional time of flight (3D TOF),
phase-contrast (PC), and contrast-enhanced MRA
(CEMRA). Three-dimensional TOF takes advantage
of the higher signal from protons in flowing blood,
compared with protons in stationary tissue, which
become partially saturated and lose signal when
exposed to a radiofrequency (RF) pulse. Areas of
signal loss and narrowing correspond to stenosis and
occlusions. PC involves tagging the spins of moving
protons using bidirectional gradients and marking
their changes in position when each gradient is
applied. PC is exquisitely sensitive to flow, which the
operator can choose the velocity threshold for, and
gives excellent background suppression. CEMRA
utilizes the intraluminal signal produced by a timed
bolus of paramagnetic contrast material to evaluate
vessel patency. Images may be single phase (i.e.
arterial) or time resolved.
For more information, see Magnetic Resonance
Imaging in Acute Stroke.
CT scanning
Imaging with computed tomography (CT) scanning
has multiple logistic advantages for patients with
acute stroke. CT scanning is able to more rapidly
acquire images than MRI, allowing for assessment
with an examination that includes noncontrast CT
scanning, CT angiography, CT perfusion scanning in
less than 10 minutes. Expedient acquisition is of the
 utmost importance in acute stroke imaging because
of the narrow window of time available for definitive
ischemic stroke treatment with pharmacologic
agents and mechanical devices. CT scanning can also
be performed in patients who are unable to tolerate
an MR examination or who have contraindications to
MRI, including pacemakers, aneurysm clips, or other
ferromagnetic materials in their bodies. Additionally,
CT scanning is more easily accessible for patients
who require special equipment for maintaining and
monitoring life support.[52, 53]
The 2011 AHA/ASA CVT statement notes that MRI
is more sensitive for the detection of CVT than CT.
However, these modalities do not always accurately
reveals positive findings of intraluminal thrombus,
which is key to the diagnosis of CVT. Therefore,
although a plain CT or MRI is useful in the initial
evaluation, a negative finding should not rule out
CVT.[46]
Other imaging studies in ischemic stroke
Transcranial Doppler ultrasonography is useful for
evaluating more proximal vascular anatomy through
the infratemporal fossa, including the MCA,
intracranial carotid artery, and vertebrobasilar
artery.[54]
Echocardiography is obtained in all patients with
acute ischemic stroke in whom cardiogenic embolism
is suspected.
Chest radiography has potential utility for patients
with acute stroke. However, obtaining a chest
radiograph should not delay the administration of
recombinant tissue-type plasminogen activator (rt-
PA); these radiographs have not been shown to alter
the clinical course or decision-making in most
cases.[55]
The use of SPECT scanning in stroke is still
relatively experimental and available only at select
institutions; it can theoretically define areas of
altered regional blood flow.
Conventional angiography is the gold standard in
evaluating for cerebrovascular disease as well as for
disease involving the aortic arch and great vessels in
the neck; it also provides for less invasive
endovascular interventions. Conventional angiography
can be performed to clarify equivocal findings or to
confirm and treat disease seen on MRA, CTA,
transcranial Doppler or ultrasonography of the neck.
Lumbar Puncture
A lumbar puncture is required to rule out meningitis
or subarachnoid hemorrhage when the CT scan is
negative but the clinical suspicion remains high.
Approach Considerations
Multiple factors contribute to delays in seeking care for
symptoms of stroke. Many strokes occur while patients are
sleeping (also known as "wake-up" stroke) and are not
discovered until the patient wakes. Stroke can leave some
patients too incapacitated to call for help. Occasionally, a
stroke goes unrecognized by the patient or their caregivers.
(See Diagnostic Considerations).[36, 56]
The median time from symptom onset to ED presentation
ranges from 4-24 hours in the United States.[22] Prehospital
care providers are essential to timely stroke care. Course
curricula for prehospital care providers are beginning to
include more information on stroke than ever before.
Through certification and ACLS instruction, as well as
continuing medical education classes, prehospital care
providers can remain current on stroke and promote stroke
awareness in their own communities.
Physician and nursing staff involved in the care of patients
who have had a stroke, in the ED and in the hospital, should
participate in scheduled stroke education. This will help them
to maintain the skills required to treat stroke patients
effectively and to remain current on medical advances for all
stroke types.
Establishing the time at which stroke symptoms first
occurred is of paramount importance when considering
patients for possible thrombolytic therapy. An essential
question is, "When was the patient last seen to be normal?"
It is advisable for emergency clinicians to rapidly enlist the
assistance of family members or relatives to establish time
of symptom onset and to identify other pertinent components
of the patient's presentation history.
The central goal of therapy in acute ischemic stroke is to
preserve the area of oligemia in the ischemic penumbra. The
area of oligemia can be preserved by limiting the severity of
ischemic injury (ie, neuronal protection) or by reducing the
duration of ischemia (ie, restoring blood flow to the
compromised area).
Recanalization strategies, including IV recombinant tissue-
type plasminogen activator (rt-PA) and intra-arterial
approaches, attempt to establish revascularization so that
cells in the penumbra can be rescued before irreversible
injury occurs. Restoring blood flow can mitigate the effects
of ischemia only if performed quickly. Neuroprotective
strategies are intended to preserve the penumbral tissues
and to extend the time window for revascularization
techniques; however, at the present time, no neuroprotective
agents are available and approved for use in ischemic stroke.
The ischemic cascade offers many points at which such
interventions could be attempted. Multiple strategies and
interventions for blocking this cascade are currently under
investigation. The timing of the restoration of cerebral blood
flow appears to be a critical factor. Time may also prove to
be a key factor in neuronal protection. It is expected that
neuroprotective agents, which block the earliest stages of
the ischemic cascade (eg, glutamate receptor antagonists,
calcium channel blockers), will be effective only in the
proximal phases of presentation.
The American Heart Association (AHA) and American Stroke
Association (ASA) released new guidelines for the early
management of acute ischemic stroke in January 2013. New
features of the guidelines include a focus on the importance
of stroke systems of care, a recommendation for the use of
tissue plasminogen activator (t-PA) in selected patients
presenting within 3 to 4.5 hours of symptom onset, and a
recommendation for door-to-needle times within 60 minutes
of hospital arrival in patients eligible for thrombolysis.[27, 3]
A registry study involving 58,353 patients with acute
ischemic stroke who underwent t-PA treatment within 4.5
hours of symptom onset confirmed that earlier treatment
yielded better outcomes.[57, 58] For every 1000 patients, the
investigators found that with each 15-minute reduction in
time to therapy, an additional 18 patients had improved
ambulation at discharge, an additional 13 patients were
discharged to a more independent environment, and an
additional 4 patients survived to discharge.
Emergency Response and Transport
Recognition that a stroke may have occurred and rapid
transport to the appropriate receiving facility are necessary
after addressing the ABCs. Of patients with signs or
symptoms of stroke, 29-65% utilize some facet of the
emergency medical services (EMS) system.[59,
60]
Furthermore, most patients who call EMS are those who
present within 3 hours of symptom onset. EMS use is
associated with shorter time periods from symptom onset to
hospital arrival.[61, 62]
Stroke should be a priority dispatch with prompt EMS
response. EMS responders should provide in as timely a
manner as possible advance notice to their emergency
department destination so as to allow preparation and
marshaling of personnel and resources. There is now ongoing
development of stroke center designation that would then
become the preferred destination for patients with acute
stroke symptoms utilizing EMS.
Data supporting the use of emergency air transport for
patients with acute stroke symptoms are limited. Further
evaluation of this transportation modality is necessary to
minimize the potentially high number of stroke mimics and to
maximize the appropriate use of transport resources.
Telemedicine is also a technology that has the potential to
provide timely expert advice to rural and underserved clinics
and hospitals.[22]
Acute Management of Stroke
The goal for the acute management of patients with stroke is
to stabilize the patient and to complete initial evaluation and
assessment, including imaging and laboratory studies within
60 minutes of patient arrival.[22] A Finnish study
demonstrated that time to treatment with thrombolytics can
be decreased with changes in EMS and ED coordination and in
ED procedures for treating acute stroke patients.[63] Critical
decisions focus on blood pressure control, the need for
intubation, and determination of risk-to-benefit profile for
thrombolytic intervention. Referral to a physician with a
special interest in stroke is ideal. Stroke care units exist and
improve outcomes with specially trained personnel.
Comorbid medical problems need to be addressed.
Hypoglycemia and hyperglycemia need to be identified and
treated early in the evaluation. Hyperthermia is infrequently
associated with stroke but can increase morbidity.
Administration of acetaminophen, by mouth or per rectum, is
indicated in the presence of fever (temperature >100.4F).
Supplemental oxygen is recommended when the patient has a
documented oxygen requirement. In the small proportion of
patients with stroke who are relatively hypotensive,
pharmacologically increasing blood pressure may improve flow
through critical stenoses.
An area of continued interest in acute stroke is glucose
management. A Cochrane review found that the use of
intravenous insulin to maintain serum glucose within the first
few hours of ischemic stroke did not improve functional
outcome, death, or final neurological deficit and significantly
increased the risk of hypoglycemia.[64]
The 2011 AHA/ASA statement on CVT notes that
appropriate acute therapy should focus on preventing
complications and anticoagulation therapy. The recommended
tests were MRI and MR venography (MRV) because they are
the most sensitive. Blood workup should be performed later
based on the underlying causes.[46]
Thrombolytic Therapy
Thrombolytics restore cerebral blood flow among some
patients with acute ischemic stroke and may lead to
improvement or resolution of neurologic deficits.
Unfortunately, thrombolytics can also cause symptomatic
intracranial hemorrhage, defined as radiographic evidence of
hemorrhage combined with escalation of the NIHSS score by
4 or more points (see the NIH Stroke Scorecalculator).
Therefore, if the patient is a candidate for thrombolytic
therapy, a thorough review of the inclusion and exclusion
criteria must be performed. The exclusion criteria largely
focus on identifying risk of hemorrhagic complication
associated with thrombolytic use.
While streptokinase and rt-PA have been shown to benefit
patients with acute MI, only alteplase (rt-PA) has been shown
to benefit selected patients with acute ischemic stroke.
In May 2009, the American Heart Association/American
Stroke Association (AHA/ASA) guidelines for the
administration of rt-PA following acute stroke were revised
to expand the window of treatment from 3 hours to 4.5 hours
to provide more patients with an opportunity to receive
benefit from this effective therapy.[8, 9, 65] Eligibility criteria
for treatment in the 3-4.5 hours after acute stroke are
similar to those for treatment at earlier time periods, with
any 1 of the following additional exclusion criteria:
Patients older than 80 years
All patients taking oral anticoagulants are excluded
regardless of the international normalized ratio (INR)
Patients with baseline NIHSS greater than 25
Patients with a history of stroke and diabetes
Caution should be exercised in the administration of rt-PA to
patients with major deficits. Patients with evidence of low
attenuation (edema or ischemia) involving more than a third
of the distribution of the MCA on their initial NCCT scan are
less likely to have favorable outcome after thrombolytic
therapy and are thought to be at higher risk for hemorrhagic
transformation of their ischemic stroke.[38] In addition to the
risk of symptomatic intracranial hemorrhage (6.4% in the
NINDS trial), other complications include potentially
hemodynamically significant hemorrhage and angioedema or
allergic reactions.[22]
Streptokinase has not been shown to benefit patients with
acute ischemic stroke, but it has been shown to increase
their risk of intracranial hemorrhage and death.
Researchers have studied the use of transcranial ultrasound
as a means of assisting rt-PA in thrombolysis. By delivering
mechanical pressure waves to the thrombus, ultrasound can
theoretically expose more of its surface to the circulating
thrombolytic agent. Further research is necessary to
determine the exact role of transcranial Doppler ultrasound
in assisting thrombolytics in acute ischemic stroke.
No human trials comparing the IV versus intra-arterial
administration of thrombolytics exist. Theoretic advantages
to intra-arterial delivery may include the possibility that
higher local concentrations of thrombolytic would allow lower
total doses of the agent (and theoretically less risk of
systemic bleed) and a longer therapeutic window; however,
the longer time to administration via the intra-arterial
approach versus the IV approach may mitigate some of this
advantage.
For more information, see Thrombolytic Therapy.
For more information, see Reperfusion Injury in Stroke.
Antiplatelet Agents
The International Stroke Trial and the Chinese Acute Stroke
Trial (CAST) demonstrated modest benefit from the use of
aspirin in the setting of acute ischemic stroke. The
International Stroke Trial randomized 20,000 patients within
48 hours of stroke onset to treatment with aspirin 325 mg,
subcutaneous heparin in 2 different dose regimens, aspirin
with heparin, and a placebo. The study found that aspirin
therapy reduced the risk of early stroke recurrence.[3, 4]
CAST evaluated 21,106 patients and had a 4-week mortality
reduction of 3.3% contrasted to 3.9%. A separate study also
found that the combination of aspirin and lowmolecular-
weight heparin did not significantly improve outcomes.[3]
The early initiation of aspirin plus extended-release
dipyridamole is likely to be as safe and effective in
preventing disability as is later initiation after 7 days
following stroke onset, according to a German study. The
studys authors attempted to assess the precise time to
initiate dipyridamole following ischemic stroke or
TIA.[66] Patients from 46 stroke units who presented with an
NIHSS score of 20 or less were randomly assigned to
receive aspirin 25 mg plus extended-release dipyridamole
200 mg bid (early dipyridamole regimen) (n=283) or aspirin
monotherapy (100 mg once daily) for 7 days (n=260). Therapy
in either group was initiated within 24 hours of stroke onset.
After 2 weeks, all patients received aspirin plus dipyridamole
for up to 90 days. At day 90, 154 (56%) patients in the early
dipyridamole group and 133 (52%) in the aspirin plus later
dipyridamole group had no or mild disability (P = .45).
Other antiplatelet agents are also under evaluation for use in
the acute presentation of ischemic stroke. In a preliminary
pilot study, abciximab was given within 6 hours to establish a
safety profile. A trend toward improved outcome at 3 months
for the treatment versus the placebo group was
noted.[67] Further clinical trials are necessary.
Neuroprotective Agents
Despite very promising results in several animal studies, as of
yet no single neuroprotective agent in ischemic stroke is
supported by randomized, placebo-controlled human studies.
Nevertheless, substantial research is underway evaluating
different neuroprotective strategies, including hypothermia.
For more information, see Neuroprotective Agents in Stroke.
Mechanical Thrombolysis
Studies have evaluated the efficacy of mechanical clot
disruption in the setting of acute stroke. In most cases,
these technologies were used in combination with
thrombolysis. In an investigation by Berlis et al, mechanical
disruption via an endovascular photoacoustic device was found
to be more effective than thrombolysis alone in
recanalization rates.[68]
There are currently 2 FDA-approved devices for the
endovascular treatment of acute ischemic stroke: the
Concentric Retriever, which is mainly a grasping device, and
the Penumbra device, which employs an aspiration function to
remove clots.[69, 70, 71] The Penumbra trial demonstrated 82%
recanalization in patients when using the aspiration function
of the Penumbra device.
Successful recanalization occurred in 12 of 28 patients in the
Mechanical Embolus Retrieval in Cerebral Ischemia (MERCI) 1
pilot trial, a study of the Merci Retrieval System.[72]
In a second MERCI study, recanalization was achieved in 48%
of those in which the device was deployed. Clot was
successfully retrieved from all major cerebral arteries;
however, the recanalization rate for the MCA was lowest. A
further study of clot extraction, the Prolyse in Acute
Cerebral Thromboembolism II (PROACT II) study, identified
a recanalization rate of 66%.[73, 74]
The Multi MERCI trial used the newer generation Concentric
retrieval device (L5). Recanalization was demonstrated in
approximately 55% of patients who did not receive t-PA and
in 68% of those for whom t-PA was given in a group of
patients with acute ischemic stroke presenting within 8 hours
of onset of symptoms. Seventy-three percent of patients
who failed IV t-PA therapy had recanalization following
mechanical embolectomy.[75] However, based on these results,
the FDA has cleared the use of the MERCI device in patients
who are either ineligible for or who have failed IV
thrombolytics.
According to the 2011 AHA/ASA statement on CVT, evidence
is insufficient to draw conclusions about the value of
endovascular thrombolysis in patients with CVT. For that
reason, the statement recommends this therapy only in
patients with progressive neurological deterioration that
persists despite medical treatment.[46]
For more information, see Mechanical Thrombolysis in Acute
Stroke.
For more information, see Cerebral Revascularization.
Fever Control
Antipyretics are indicated for febrile stroke patients, since
hyperthermia accelerates ischemic neuronal injury.
Substantial experimental evidence suggests that mild brain
hypothermia is neuroprotective. The use of induced
hypothermia is currently being evaluated in phase I clinical
trials.[76, 77, 78]
High body temperature in the first 12-24 hours after stroke
onset has been associated with poor functional outcome.
Results from the Paracetamol (Acetaminophen) In Stroke
(PAIS) trial did not support the routine use of high-dose
acetaminophen in patients with acute stroke. The study
assessed whether early treatment with paracetamol improves
functional outcome in patients with acute stroke by reducing
body temperature and preventing fever. Patients (n=1400)
were randomly assigned to receive acetaminophen (6 g daily)
or placebo within 12 hours of symptom onset. After 3
months, improvement on the modified Rankin scale was not
beyond what was expected.[79]
Cerebral Edema Control
Significant cerebral edema after ischemic stroke is thought
to be somewhat rare (10-20%); maximum severity of edema is
reached 72-96 hours after the onset of stroke.
Early indicators of ischemia on presentation and on NCCT
scans are independent indicators of potential swelling and
deterioration. Mannitol and other therapies to reduce ICP
may be used in emergency situations, although their
usefulness in swelling secondary to ischemic stroke is
unknown. No evidence exists supporting the use of
corticosteroids to decrease cerebral edema in acute ischemic
stroke. Prompt neurosurgical assistance should be sought
when indicated.[22]
Patient position, hyperventilation, hyperosmolar therapy, and,
rarely, barbiturate coma may be used, as in patients with
increased ICP secondary to closed head injury.
Hemicraniectomy has shown to decrease mortality and
disability among patients with large hemispheric infarctions
associated with life-threatening edema.[80, 81, 82, 83]
Seizure Control
Seizures occur in 2-23% of patients within the first days
after stroke. Although seizure prophylaxis is not indicated,
prevention of subsequent seizures with standard antiepileptic
therapy is recommended.[22]
The 2011 AHA/ASA CVT statement notes a lack of clinical
trials on the use of anticonvulsants to control seizures, which
occur in 37% of adults, 48% of children, and 71% of
newborns who present with CVT. Therefore, opinions on their
use vary greatly. However, because seizures increase the risk
of anoxic damage, anticonvulsant treatment after even a
single seizure is reasonable.[46]
Post-ischemia strokes are usually focal, but they may be
generalized. A fraction of patients who have experienced
stroke develop chronic seizure disorders. Seizures secondary
to ischemic stroke should be managed in the same manner as
other seizure disorders that arise as a result of neurologic
injury.[22]
Acute Decompensation or Escalation
In the case of the rapidly decompensating patient or the
patient with deteriorating neurologic status, reassessment of
ABCs as well as hemodynamics and reimaging are indicated.
Many patients who develop hemorrhagic transformation or
progressive cerebral edema will demonstrate acute clinical
decline. Rarely, a patient may have escalation of symptoms
secondary to increased size of the ischemic penumbra. Some
advocate resetting the time window to zero in this
circumstance and encourage consideration of reperfusion
strategies.
Anticoagulation and Prophylaxis
Heparin is known to prolong the lytic state caused by t-PA.
Currently, data are inadequate to justify the utilization of
heparin or other anticoagulants in the acute management of
patients with ischemic stroke. Patients with embolic stroke
who have another indication for anticoagulation (eg, atrial
fibrillation) may be placed on anticoagulation therapy with
the goal of preventing further embolic disease; however, the
potential beneficial effects from that decision must be
weighted against the risk of hemorrhagic transformation.[22]
Immobilized stroke patients who are not receiving
anticoagulants, such as IV heparin or an oral anticoagulant,
may benefit from the administration of low-dose,
subcutaneous unfractionated or lowmolecular-weight
heparin, which reduces the risk of deep venous
thrombosis.[22]
For more information, see Stroke Anticoagulation and
Prophylaxis.
Induced Hypothermia
Hypothermia is fast becoming the standard of care for the
ongoing treatment of patients surviving cardiac arrest due to
ventricular tachycardia or ventricular fibrillation. However,
no major clinical study has demonstrated a role for
hypothermia in the early treatment of ischemic stroke.[22]
Carotid Endarterectomy
Many surgical and endovascular techniques have been studied
in the treatment of acute ischemic stroke. Carotid
endarterectomy has been used with some success in the
acute management of internal carotid artery occlusions, but
no evidence supports its use in acute stroke.
Stroke Prevention
Primary prevention refers to the treatment of individuals
with no previous history of stroke. Measures may include the
use of platelet antiaggregants; 3-hydroxy-3-methylglutaryl
coenzyme A (HMG-CoA) reductase inhibitors (ie, statins); and
exercise. In February 2011, AHA/ASA guidelines for the
primary prevention of stroke were published. The guideline
emphasizes the importance of lifestyle changes to reduce
well-documented modifiable risk factors, citing an 80% lower
risk of a first stroke in people who follow a healthy lifestyle
compared with those who do not.[84]
Secondary prevention refers to the treatment of individuals
who have already had a stroke. Measures may include the use
of platelet antiaggregants, antihypertensives, HMG-CoA
reductase inhibitors (statins), and lifestyle interventions.
Smoking cessation, blood pressure control, diabetes control,
a low-fat diet, weight loss, and regular exercise should be
encouraged as strongly as the medications described above.
Written prescriptions for exercise and medications for
smoking cessation (nicotine patch, bupropion, varenicline)
increase the likelihood of success with these interventions.
In addition to these well-documented factors, the 2011
AHA/ASA guidelines for primary stroke prevention indicate
that it is reasonable to avoid exposure to environmental
tobacco smoke despite a lack of stroke-specific data.
 The use of aspirin for primary stroke prevention is not
recommended for persons at low risk. Aspirin is
recommended for this purpose only in persons with at least a
6-10% risk of cardiovascular events over 10 years.[84]
For patients with stroke risk due to asymptomatic carotid
artery stenosis, the 2011 AHA/ASA primary prevention
guidelines state that older studies that showed
revascularization surgery as more beneficial than medical
treatment may now be obsolete due to improvements in
medical therapies. Therefore, individual patient
comorbidities, life expectancy, and preferences should
determine whether medical treatment alone or carotid
revascularization is selected.[84]
Atrial fibrillation is a major risk factor for stroke. The 2011
ACC Foundation (ACCF)/AHA/Heart Rhythm Society (HRS)
atrial fibrillation guideline update on dabigatran states that
the new anticoagulant dabigatran is useful as an alternative
to warfarin in patients with atrial fibrillation who do not have
a prosthetic heart valve or hemodynamically significant valve
disease.[85]
The 2011 AHA/ASA primary stroke prevention guideline
recommends that EDs screen for AF and assess patients for
anticoagulation therapy if AF is found.[84]
For patients with atrial fibrillation after stroke or TIA, the
2010 AHA/ASA secondary stroke prevention guideline is in
accord with the standard recommendation of warfarin, with
aspirin as an alternative for patients who cannot take oral
anticoagulants. However, clopidogrel should not be used in
combination with aspirin for such patients because the
bleeding risk of the combination is comparable to that of
warfarin. The guideline states that the benefit of warfarin
after stroke or TIA in patients without atrial fibrillation has
not been established.[86]
The 2011 AHA/ASA guideline recommends ED-based smoking
cessation interventions, and considers it reasonable for EDs
to screen patients for hypertension and drug abuse.[84]
Periprocedural use of antithrombotic medications
In May 2013, the American Academy of Neurology issued
guidelines on the periprocedural management of
antithrombotic medications in patients with ischemic
cerebrovascular disease.[87, 88]
The guidelines list all the procedures for which there are
data on stopping or continuing aspirin or warfarin and give
recommendations. Key recommendations include the
following:
Stroke patients who are undergoing dental procedures
should continue aspirin
Stroke patients who are undergoing invasive ocular
anesthesia, cataract surgery, dermatologic procedures,
spinal/epidural procedures, transrectal ultrasound-guided
prostate biopsy, or carpal tunnel surgery should probably
continue aspirin
Stroke patients receiving warfarin should routinely
continue treatment when undergoing dental procedures and
should probably continue treatment during dermatologic
procedures
Neurologists should counsel patients that bridging therapy
is probably associated with increased bleeding risks, as
compared with stopping warfarin; the risks compared with
continuing warfarin are unknown
Specialized Stroke Centers
Given the multitude of factors that go into the care of a
patient with acute stroke, the concept of the specialized
stroke center has evolved. The Brain Attack Coalition
provided recommendations for the establishment of 2 tiers
of stroke centers: primary stroke centers (PSCs) and
comprehensive stroke centers (CSCs).[22] The Joint
Commission for the Accreditation of Hospital Organizations
(JCAHO) now provides accreditation for PSC, and efforts to
establish the requirements that distinguish CSC are
currently ongoing.
The PSC is designed to maximize the timely provision of
stroke-specific therapy, including the administration of rt-
PA, and is also capable of providing care to patients with
uncomplicated stroke. The CSC shares the commitment that
the PSC has to acute delivery of rt-PA and also provides care
to patients with hemorrhagic stroke and intracranial
hemorrhage and all patients with stroke requiring ICU level
of care.[22]
Once patients have been identified as potential stroke
patients, their ED evaluation must be fast-tracked to allow
for the completion of required laboratory tests and requisite
noncontrast head CT scanning, as well as the notification and
involvement of neurologic consultation. These requirements
have led to the development of "stroke codes" or "stroke
activations" in which EMS crews have been trained to
identify possible stroke patients and arrange for their
speedy, preferential transport to a PSC or CSC.
Additionally, Stroke Centers should have personnel versed at
monitoring stroke vital signs, which include the following:
Blood pressure
Glucose levels
Temperature
Oxygenation
Change in neurologic status
Hospitals with specialized stroke teams have demonstrated
significantly increased rates of thrombolytic administration
and decreased mortality. Cumulatively, the center should
identify performance measures and include mechanisms for
evaluating the effectiveness of the system as well as its
component parts. The acute care of the stroke patient is
more than anything a systems-based team approach requiring
the cooperation of the ED, radiology, pharmacy, neurology,
and ICU staff.
A stroke system should ensure effective interaction and
collaboration among the agencies, services, and people
involved in providing prevention and the timely identification,
transport, treatment, and rehabilitation of stroke patients.
For more information, see Stroke Team Creation and Primary
Stroke Center Certification.
Palliative Care
Palliative care is an important component of comprehensive
stroke care. Some stroke patients will simply not recover,
and others will be in a state of debilitation such that the
most humane and appropriate therapeutic concern is the
comfort of the patient. Some patients have advanced
 directives providing instructions for medical providers in the
event of severe medical illness or injury.
Consultations
Consultations are tailored to individual patient needs.
An experienced professional who is sufficiently familiar with
stroke or a stroke team should be available within 15 minutes
of the patient's arrival in the ED. Often, occupational
therapy, physical therapy, speech therapy, and physical
medicine and rehabilitation experts are consulted within the
first day of hospitalization. Consultation of cardiology and
vascular surgery or neurosurgery may be warranted based on
the results of carotid duplex scanning , neuroimaging,
transthoracic and transesophageal echocardiography, and
clinical course. During hospitalization, additional useful
consultations include the following:
Home health care coordinator
Rehabilitation coordinator
Social worker
Psychiatrist (commonly for depression)
Dietitian
Medication Summary
While only 1 drug, tissue plasminogen activator (t-PA), has
demonstrated efficacy and effectiveness in treating acute
ischemic stroke (AIS) and is approved by the US Food and
Drug Administration (FDA), other medications are equally
important. National consensus panels have included
antihypertensives, anticonvulsants, and osmotic agents in
their recommendations. Additional agents may be required
for comorbid illnesses in many patients with stroke.
Medications for the management of ischemic stroke can be
distributed into the following categories:
Anticoagulation
Reperfusion
Antiplatelet
Neuroprotective
Fibrinolytic Agents
Class Summary
Fibrinolytic agents convert entrapped plasminogen to plasmin
and initiate local fibrinolysis by binding to fibrin in a clot.
View full drug information
Alteplase (Activase)
Alteplase is a t-PA used in management of acute MI, acute
ischemic stroke, and pulmonary embolism. Safety and
efficacy with concomitant administration of heparin or
aspirin during the first 24 hours after symptom onset have
not been investigated.
Anticonvulsant Agents
Class Summary
While seizures associated with stroke are relatively
uncommon, recurrent seizures may be life threatening.
Generally, agents used for treating recurrent convulsive
seizures are also used in patients with seizures after stroke.
Benzodiazepines, typically diazepam and lorazepam, are the
first-line drugs for ongoing seizures.
View full drug information
Diazepam (Valium)
Diazepam acts on the gamma-aminobutyric acid (GABA)
receptor complex in the limbic system and thalamus,
producing a calming effect. The drug is useful in controlling
active seizures and should be augmented by longer-acting
anticonvulsants, such as phenytoin or phenobarbital.
View full drug information
Lorazepam (Ativan)
Lorazepam is a short-acting benzodiazepine with a
moderately long half-life. It has become drug of choice in
many centers for treating active seizures.
Antiplatelet Agents
Class Summary
Although antiplatelet agents have been shown useful for
preventing recurrent stroke or stroke after transient
ischemic attacks (TIAs), efficacy in the treatment of acute
ischemic stroke has not been demonstrated. Early aspirin
therapy is recommended within 48 hours of the onset of
symptoms but should be delayed for at least 24 hours after
rt-PA administration. Aspirin should not be considered as an
alternative to IV thrombolysis or other therapies aimed at
improving outcomes after stroke.
View full drug information
Aspirin (Bayer Aspirin, Anacin, Bufferin)
Aspirin blocks prostaglandin synthetase action, which in turn
inhibits prostaglandin synthesis and prevents the formation
of platelet-aggregating thromboxane A2. It also acts on the
hypothalamic heat-regulating center to reduce fever.
View full drug information
Ticlopidine (Ticlid)
Ticlopidine is a second-line antiplatelet therapy for patients
who cannot tolerate aspirin or in whom aspirin is not
effective.
View full drug information
Dipyridamole and aspirin (Aggrenox)
The combination of extended-release dipyridamole and
aspirin reduces the relative risk of stroke, death, and MI. It
is used for the secondary prevention of ischemic stroke and
TIAs.
View full drug information
Clopidogrel (Plavix)
Clopidogrel inhibits platelet aggregation and is used for
secondary stroke prevention. It is indicated for the
reduction of atherothrombotic events following a recent
stroke.
Anticoagulants
Class Summary
Anticoagulants such as warfarin are used for secondary
stroke prevention.
View full drug information
Warfarin (Coumadin, Jantoven)
Warfarin is a coumarin anticoagulant used to reduce the risk
of death, recurrent MI, and thromboembolic events such as
stroke or systemic embolization after MI.
Antipyretic Agents
Class Summary
Hyperthermia in acute stroke is potentially harmful and
should be treated. Agents with potential bleeding risk should
be avoided if possible.
View full drug information
Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

Acetaminophen reduces fever by acting directly on

hypothalamic heat-regulating centers, which increases the
dissipation of body heat via vasodilation and sweating.
Antihypertensive Agents
Class Summary
Optimal blood pressure management in acute stroke remains
subject to some debate. Treatment parameters largely
depend on whether the patient is a candidate for
thrombolytic therapy. While the target blood pressures may
differ, the therapeutic agents are largely the same.
View full drug information
Labetalol (Normodyne)

Labetalol is an adrenergic receptor-blocking agent with

nonselective beta-adrenergic and selective alpha1 competitive
receptor-blocking actions. It produces dose-related
decreases in blood pressure without inducing reflex
tachycardia.
View full drug information
Enalapril (Vasotec)

An ACE inhibitor, enalapril decreases circulating angiotensin

II levels and suppresses the renin-angiotensin-aldosterone
system, lowering overall blood pressure.
View full drug information
Nicardipine (Cardene)

A calcium-channel blocker, nicardipine inhibits calcium ion

influx into vascular smooth muscle and myocardium.[89]
View full drug information
Sodium nitroprusside (Nitropress)

Sodium nitroprusside is a vasodilator that decreases

peripheral vascular resistance by direct action of arteriolar
smooth muscle. It also decreases venous return through
venous dilation.