stroke iskemik
DESCRIPTION
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1. OVERVIEW
Practice Essentials
Ischemic stroke is characterized by the sudden loss of blood circulation to an area of the brain,
resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by
thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic
stroke.
Essential update: Antihypertensive treatment found not beneficial in acute ischemic stroke
In the single-blind, randomized China Antihypertensive Trial in Acute Ischemic Stroke (CATIS)
study, which included 4,071 patients with acute ischemic stroke and elevated blood pressure,
immediate blood pressure reduction with antihypertensive medication within 48 hours of
symptom onset did not reduce the risk for death or major disability. CATIS excluded patients
who received thrombolytic therapy. Mean systolic blood pressure was reduced from 166.7 to
144.7 mm Hg within 24 hours in the antihypertensive treatment group.[1, 2]
Among the 2,038 patients who received antihypertensive treatment, 683 reached the primary
endpoint of death or major disability at 14 days or hospital discharge, compared with 681 of the
2,033 patients who received no antihypertensive treatment. At 3-month follow-up, 500 patients
in the antihypertensive treatment group and 502 patients in the control group reached the
secondary endpoint of death or major disability.[1, 2]
Signs and symptoms
Consider stroke in any patient presenting with acute neurologic deficit or any alteration in level
of consciousness. Common stroke signs and symptoms include the following:
Abrupt onset of hemiparesis, monoparesis, or (rarely) quadriparesis Hemisensory deficits Monocular or binocular visual loss Visual field deficits Diplopia
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Dysarthria Facial droop Ataxia Vertigo (rarely in isolation) Nystagmus Aphasia Sudden decrease in level of consciousness
Although such symptoms can occur alone, they are more likely to occur in combination. No
historical feature distinguishes ischemic from hemorrhagic stroke, although nausea, vomiting,
headache, and sudden change in level of consciousness are more common in hemorrhagic
strokes. In younger patients, a history of recent trauma, coagulopathies, illicit drug use
(especially cocaine), migraines, or use of oral contraceptives should be elicited.
With the availability of fibrinolytic 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 the neurologic examination include the following:
Confirming the presence of a stroke syndrome Distinguishing stroke from stroke mimics Establishing a neurologic baseline, should the patient's condition improve or deteriorate Establishing stroke severity, using a structured neurologic exam and score (National Institutes
of Health Stroke Scale [NIHSS]) to assist in prognosis and therapeutic selectionEssential
components of the neurologic examination include the following evaluations:
Cranial nerves Motor function Sensory function Cerebellar function Gait Deep tendon reflexes Language (expressive and receptive capabilities) Mental status and level of consciousness
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The skull and spine also should be examined, and signs of meningismus should be sought.
Diagnosis
Emergent brain imaging is essential for confirming the diagnosis of ischemic stroke. Noncontrast
computed tomography (CT) scanning is the most commonly used form of neuroimaging in the
acute evaluation of patients with apparent acute stroke. The following neuroimaging techniques
are also used:
CT angiography and CT perfusion scanning Magnetic resonance imaging (MRI) Carotid duplex scanning Digital subtraction angiographyLumbar 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
Laboratory studies
Laboratory tests performed in the diagnosis and evaluation of ischemic stroke include the
following:
Complete blood count (CBC): A baseline study that may reveal a cause for the stroke (eg,polycythemia, thrombocytosis, thrombocytopenia, leukemia) or provide evidence of
concurrent illness (eg, anemia)
Basic chemistry panel: A baseline study that may reveal a stroke mimic (eg, hypoglycemia,hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency)
Coagulation studies: May reveal a coagulopathy and are useful when fibrinolytics oranticoagulants are to be used
Cardiac biomarkers: Important because of the association of cerebral vascular disease andcoronary artery disease
Toxicology screening: May assist in identifying intoxicated patients with symptoms/behaviormimicking stroke syndromes
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Pregnancy testing: A urine pregnancy test should be obtained for all women of childbearingage with stroke symptoms; recombinant tissue-type plasminogen activator (rt-PA) is a
pregnancy class C agent
Arterial blood gas analysis: In selected patients with suspected hypoxemia, arterial blood gasdefines the severity of hypoxemia and may be used to detect acid-base disturbances
SeeWorkup for more detail.
Management
The goal for the emergent management of stroke is to complete the following within 60 minutes
of patient arrival[3] :
Assess airway, breathing, and circulation (ABCs) and stabilize the patient as necessary Complete the initial evaluation and assessment, including imaging and laboratory studies Initiate reperfusion therapy, if appropriate
Critical treatment decisions focus on the following:
The need for airway management
Optimal blood pressure control Identifying potential reperfusion therapies (eg, intravenous fibrinolysis with rt-PA or intra-
arterial approaches)
Involvement of a physician with a special interest in stroke is ideal. Stroke care units with
specially trained personnel exist and improve outcomes.
Ischemic stroke therapies include the following:
Fibrinolytic therapy Antiplatelet agents[4, 5] Mechanical thrombectomy
Treatment of comorbid conditions may include the following:
Reduce fever
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Correct hypotension/significant hypertension Correct hypoxia Correct hypoglycemia Manage cardiac arrhythmias Manage myocardial ischemia
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 Statins Exercise Lifestyle interventions (eg, smoking cessation, alcohol moderation)
Secondary prevention refers to the treatment of individuals who have already had a stroke.
Measures may include use of the following:
Platelet antiaggregants Antihypertensives Statins Lifestyle interventions
SeeTreatment andMedication for more detail.
Image library
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Maximum intensity projection (MIP) image from a computed
tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the
branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for
thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions,
which account for approximately one third of ischemic strokes.Background
Acute ischemic stroke (AIS) is characterized by the sudden loss of blood circulation to an area of
the brain, typically in a vascular territory, resulting in a corresponding loss of neurologic
function. Also previously called cerebrovascular accident (CVA) or stroke syndrome, stroke is a
nonspecific state of brain injury with neuronal dysfunction that has several pathophysiologic
causes. Strokes can be divided into 2 types: hemorrhagic or ischemic. Acute ischemic stroke is
caused by thrombotic or embolic occlusion of a cerebral artery. (See the image below.)
Maximum intensity projection (MIP) image from a computed
tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the
branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for
thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions,
which account for approximately one third of ischemic strokes.
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Nearly 800,000 people suffer strokes each year in the United States; 82-92% of these strokes are
ischemic. Stroke is the fourth leading cause of adult death and disability, resulting in over $72
billion in annual cost.[6]
Ischemic and hemorrhagic stroke cannot be reliably differentiated on the basis of clinical
examination findings alone. Further evaluation, especially with brain imaging tests (ie, computed
tomography [CT] scanning or magnetic resonance imaging [MRI]), is required. (See Workup.)
Stroke categories
The system of categorizing stroke developed in the multicenter Trial of ORG 10172 in Acute
Stroke Treatment (TOAST) divides ischemic strokes into the following 3 major subtypes[4] :
Large-artery Small-vessel, or lacunar Cardioembolic infarction
Large-artery infarctions often involve thrombotic in situ occlusions on atherosclerotic lesions in
the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches; however,
large-artery infarctions may also be cardioembolic.
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.[7] (See
Pathophysiology.)
Treatment
Recanalization strategies, including intravenous recombinant tissue-type plasminogen activator
(rt-PA) and intra-arterial approaches, attempt to establish revascularization so that cells in the
ischemic penumbra (a metabolically active region, peripheral to the ischemic area, where blood
flow is reduced) can be rescued before irreversible injury occurs. Restoring blood flow can
mitigate the effects of ischemia only if performed quickly.
The US Food and Drug Administration (FDA) has approved the use of rt-PA in patients who
meet criteria set forth by the National Institute of Neurologic Disorders and Stroke (NINDS). In
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particular, rt-PA must be given within 3 hours of stroke onset and only after CT scanning has
ruled out hemorrhagic stroke.
On the basis of recent European data, the American Heart Association and American Stroke
Association recommended expanding the window of treatment from 3 hours to 4.5 hours, with
more stringent exclusion criteria for the later period (see Treatment). The FDA has not yet
approved rt-PA for this expanded indication, but this has become the community standard in
many institutions.
Other aspects of treatment for acute ischemic stroke include the following:
Treatment of neurologic complications
Supplemental oxygen as required Antiplatelet therapy Glycemic control Optimal blood pressure control Prevention of hyperthermia
See alsoHemorrhagic Stroke.
Anatomy
The brain is the most metabolically active organ in the body. While representing only 2% of the
body's mass, it requires 15-20% of the total resting cardiac output to provide the necessary
glucose and oxygen for its metabolism.
Knowledge of cerebrovascular arterial anatomy and the territories supplied by the cerebral
arteries is useful in determining which vessels are involved in acute stroke. Atypical patterns of
brain ischemia that do not conform to specific vascular distributions may indicate a diagnosis
other than ischemic stroke, such as venous infarction.
Arterial distributions
In a simplified model, the cerebral hemispheres are supplied by 3 paired major arteries,
specifically, the anterior, middle, and posterior cerebral arteries.
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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. (See the image below.)
Lateral view of a cerebral angiogram illustrates the branches of
the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been
described to arise distal to the anterior communicating artery or distal to the origin of the
callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as
follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior
communicating artery; A2 extends to the junction of the rostrum and genu of the corpus
callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend
posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle
overlies the opercular branches of the middle cerebral artery (MCA), with the apex representing
the Sylvian point.
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 MCA is the dominant source
of vascular supply to the hemispheres. (See the images below.)
The supratentorial vascular territories of the major cerebral
arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images
through the level of the basal ganglia and thalami. The middle cerebral artery (MCA; red)
supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior
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temporal lobes; insula; and basal ganglia. The anterior cerebral artery (ACA; blue) supplies the
medial frontal and parietal lobes. The posterior cerebral artery (PCA; green) supplies the thalami
and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the
posterior limb of the internal capsule and part of the hippocampus extending to the anterior and
superior surface of the occipital horn of the lateral ventricle. Frontal view of
a cerebral angiogram with selective injection of the left internal carotid artery (ICA) illustrates
the anterior circulation. The anterior cerebral artery (ACA) consists of the A1 segment proximal
to the anterior communicating artery, with the A2 segment distal to it. The middle cerebral artery
(MCA) can be divided into 4 segments: the M1 (horizontal segment) extends to the anterior basal
portion of the insular cortex (the limen insulae) and gives off lateral lenticulostriate branches, the
M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral
hemispheric convexities).
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. (See Table 1, below.)
The cerebellar hemispheres are supplied as follows:
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Inferiorly by the posterior inferior cerebellar artery (PICA), arising from the vertebral artery
(see the image below) Frontal projection from a right vertebral
artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the
basilar artery. The posterior inferior cerebellar arteries (PICAs) arise from the distal vertebral
arteries. The anterior inferior cerebellar arteries (AICAs) arise from the proximal basilar
artery. The superior cerebellar arteries (SICAs) arise distally from the basilar artery prior to its
bifurcation into the posterior cerebral arteries (PCAs).
Superiorly by the superior cerebellar artery Anterolaterally by the anterior inferior cerebellar artery (AICA), from the basilar artery
Table 1. Vascular Supply to the Brain(Open Table in a new window)
VASCULAR
TERRITORY
Structures Supplied
Anterior Circulation (Carotid)
Anterior Cerebral Artery Cortical branches:medial frontal and parietal lobe
Medial lenticulostriate branches: caudate head, globus pallidus,
anterior limb of internal capsule
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Middle Cerebral Artery Cortical branches:lateral frontal and parietal lobes lateral and
anterior temporal lobe
Lateral lenticulostriate branches: globus pallidus and putamen,
internal capsule
Anterior Choroidal
Artery
Optic tracts, medial temporal lobe, ventrolateral thalamus, corona
radiata, posterior limb of the internal capsule
Posterior Circulation (Vertebrobasilar)
Posterior Cerebral
Artery
Cortical branches:occipital lobes, medial and posterior temporal
and parietal lobes
Perforating branches:brainstem, posterior thalamus and
midbrain
Posterior Inferior
Cerebellar Artery
Inferior vermis; posterior and inferior cerebellar hemispheres
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Anterior Inferior
Cerebellar Artery
Anterolateral cerebellum
Superior CerebellarArtery
Superior vermis; superior cerebellum
Pathophysiology
Acute ischemic strokes result from vascular occlusion secondary to thromboembolic disease (see
Etiology). Ischemia causes cell hypoxia and depletion of cellular adenosine triphosphate (ATP).
Without ATP, there is no longer the energy to maintain ionic gradients across the cell membraneand cell depolarization. Influx of sodium and calcium ions and passive inflow of water into the
cell lead to cytotoxic edema.[8, 9, 10]
Ischemic core and penumbra
An acute vascular occlusion produces heterogeneous regions of ischemia in the affected vascular
territory. Local blood flow is limited to any residual flow in the major arterial source plus the
collateral supply, if any.
Affected regions with cerebral blood flow of lower than 10 mL/100 g of tissue/min are referred
to collectively as the core. These cells are presumed to die within minutes of stroke onset.[11]
Zones of decreased or marginal perfusion (cerebral blood flow < 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.[11]
Ischemic cascade
On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and
membrane ion-transport systems fail. Disruption of cellular metabolism also impairs normal
sodium-potassium plasma membrane pumps, producing an intracellular increase in sodium,
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which in turns increases intracellular water content. This cellular swelling is referred to as
cytotoxic edema and occurs very early in cerebral ischemia.
Cerebral ischemia impairs the normal sodium-calcium exchange protein also found on cell
plasma membranes. The resulting influx of calcium leads to the release of a number of
neurotransmitters, including large quantities of glutamate, which in turn activatesN-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.[12] 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.
This produces greater levels of brain swelling and mass effect that peak at 3-5 days and resolve
over the next several weeks with resorption of water and proteins.[13, 14]
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.[12] 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 oligodendroglial and
microglial 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, resulting from encephalomalacia and cystic
change, is eventually seen. The evolution of these chronic changes may be seen in the weeks to
months following the infarction. (See the images below.)
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Vascular distributions: Middle cerebral artery (MCA) infarction. Noncontrast computed
tomography (CT) scanning demonstrates a large acute infarction in the MCA territory involving
the lateral surfaces of the left frontal, parietal, and temporal lobes, as well as the left insular and
subinsular regions, with mass effect and rightward midline shift. There is sparing of the caudate
head and at least part of the lentiform nucleus and internal capsule, which receive blood supply
from the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of
involvement of the medial frontal lobe (anterior cerebral artery [ACA] territory), thalami, and
paramedian occipital lobe (posterior cerebral artery [PCA] territory).
Vascular distributions: Anterior cerebral artery (ACA) infarction. Diffusion-weighted image on
the left demonstrates high signal in the paramedian frontal and high parietal regions. The
opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a
larger ACA infarction involving the left paramedian frontal and posterior parietal regions. There
is also infarction of the lateral temporoparietal regions bilaterally (both middle cerebral artery
[MCA] distributions), greater on the left indicating multivessel involvement and suggesting
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emboli.The supratentorial vascular territories of the major cerebral arteries are demonstrated
superimposed on axial (left) and coronal (right) T2-weighted images through the level of the
basal ganglia and thalami. The middle cerebral artery (MCA; red) supplies the lateral aspects of
the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes; insula; and
basal ganglia. The anterior cerebral artery (ACA; blue) supplies the medial frontal and parietal
lobes. The posterior cerebral artery (PCA; green) supplies the thalami and occipital and inferior
temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal
capsule and part of the hippocampus extending to the anterior and
superior surface of the occipital horn of the lateral ventricle.Vascular distributions: Anterior
choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with
associated signal dropout on the apparent diffusion coefficient (ADC) map involving the
posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal
artery, the last branch of the internal carotid artery (ICA) before bifurcating into the anterior and
middle cerebral arteries. The anterior choroidal artery may also arise from the middle cerebralartery (MCA).
Hemorrhagic transformation of ischemic stroke
Hemorrhagic transformation represents the conversion of an ischemic infarction into an area of
hemorrhage. This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence
of fibrinolytic treatment. Hemorrhagic transformation is not always associated with neurologic
decline, with the conversion ranging from the development of small petechial hemorrhages to the
formation of hematomas that produce neurologic decline and may necessitate surgical evacuationor decompressive hemicraniectomy.
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
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barrier, red blood cells extravasate from the weakened capillary bed, producing petechial
hemorrhage or more frank intraparenchymal hematoma.[8, 15, 16]
Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days postictus, usually
within the first week. It is more commonly seen following cardioembolic strokes and is more
likely to occur with larger infarct volumes.[5, 8, 17] Hemorrhagic transformation is also more likely
following administration of rt-PA in patients whose noncontrast CT (NCCT) scans demonstrate
areas of hypodensity.[18, 19, 20]
Poststroke cerebral edema and seizures
Although clinically significant cerebral edema can occur after anterior circulation ischemic
stroke, it is thought to be somewhat rare (10-20%).[3]
Edema and herniation are the most commoncauses of early death in patients with hemispheric stroke.
Seizures occur in 2-23% of patients within the first days after ischemic stroke.[3] 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 thrombotic embolism, thrombosis in situ, or relative hypoperfusion. As blood flow
decreases, neurons cease functioning. Although a range of thresholds has been described,
irreversible neuronal ischemia and injury is generally thought to begin at blood flow rates of less
than 18 mL/100 g of tissue/min, with cell death occurring rapidly at rates below 10 mL/100 g of
tissue/min
Risk factors
Risk factors for ischemic stroke include modifiable and nonmodifiable conditions. Identificationof 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 (although there are likely many others):
Age
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Race Sex Ethnicity History of migraine headaches Fibromuscular dysplasia Heredity: Family history of stroke or transient ischemic attacks (TIAs)
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. 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.[21]
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 include the following[22] :
Hypertension (the most important) Diabetes mellitus Cardiac disease: Atrial fibrillation, valvular disease, heart failure, mitral stenosis, structural
anomalies allowing right-to-left shunting (eg, patent foramen ovale), and atrial and ventricular
enlargement
Hypercholesterolemia TIAs Carotid stenosis Hyperhomocystinemia Lifestyle issues: Excessive alcohol intake, tobacco use, illicit drug use, physical inactivity[23] Obesity Oral contraceptive use/postmenopausal hormone use Sickle cell disease
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Genetic and inflammatory mechanisms
Evidence continues to accumulate that inflammation and genetic factors have important roles in
the development ofatherosclerosis 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) cholesterol 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 disorderswith stroke as a component of the phenotype demonstrate the potency of genetics in determining
stroke risk.
A number of genes are known to increase susceptibility to ischemic stroke. Mutations to
theF2andF5 genes are relatively common in the general population and increase the risk of
thrombosis. Mutations in the following genes also are known to increase the risk of stroke:
NOS3: A nitric oxide synthetase gene; involved in vascular relaxation
[24]
ALOX5AP: Involved in the metabolism of arachidonic acid[25] PRKCH: Involved in major signal transduction systems[26]Hyperhomocysteinemia and homocystinuria
Hyperhomocysteinemia is implicated in the pathogenesis of ischemic stroke. The most common
concern is mutations in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene. In many
populations, the mutant allele frequency reaches polymorphic proportions, and the risk factor for
cerebrovascular disease is related to the serum level of homocysteine. Furthermore, in persons
who are compound heterozygotes forMTHFRmutation, if elevated homocysteine is found it can
be lowered with oral folic acid therapy.
In addition, hyperhomocysteinemia can be seen in cystathione beta synthetase (CBS) deficiency,
which is generally referred to as homocystinuria. This disorder is inherited in an autosomal
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recessive manner. Symptoms usually manifest early in life. Patients have a marfanoid habitus,
ectopia lentis, and myopia and generally have intellectual disability.[27]
Thromboembolic events are the most common cause of death for patients with homocystinuria
and may be of any type, including myocardial infarction. The risk of having a vascular event in
homocystinuria is 50% by age 30.[28] It was previously suggested that persons who are
heterozygous for mutations in the CBS gene may have an increased risk of cerebrovascular
disease as well, but several more recent studies on this subject failed to replicate this finding.
Amyloid angiopathies
Amyloid angiopathies are also known to increase risk for stroke and dementia. Mutations in
the CST3gene are causative and are inherited in an autosomal dominant manner. Sufferers will
have diffuse deposition of amyloid, including in the brain. The onset of symptoms is typically in
the third or fourth decade of life, with death occurring before age 60 years. These angiopathies
appear to be most common in the Icelandic population.[29]
CADASIL
Cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy
(CADASIL), is caused by mutations in theNOTCH3 gene. It affects the small arteries of the
brain. Strokelike episodes typically occur at a mean age of 46 years, with an age range of 19-67
years. White-matter changes in the brain are typically evident by young adulthood and progress
over time.[30]
Migraine headaches occur in 30-40% of people with CADASIL. Approximately 60% of
symptomatic individuals have cognitive deficits, which can start as early as age 35 years, and
many develop multi-infarct dementia.[31]
Other mutations
Genome-wide association studies have revealed additional loci that are commonly associated
with ischemic stroke. Early onset ischemic stroke has been found to be associated with 2 single-
nucleotide polymorphisms on 2q23.3.[32]
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Large-vessel stroke has been associated with variations inHDAC9,PITX2,
andZFHX3.[33]HDAC9is located on7p21.1, whilePITX2andZFHX3are located on 9p21. It is of
note that the 9p21 locus has also been associated with cardiovascular disease.
A polymorphism at 2q36.3 was found in which adenosine substitution conferred a lower risk of
ischemic stroke in an additive fashion.[34] An additional study suggested an association between
ischemic stroke and a locus on 12p13.[35]
For more information, seeGenetic and Inflammatory Mechanisms in Stroke. In addition,
complete information on the following metabolic diseases and stroke can be found in the
following main articles:
Methylmalonic Acidemia Homocystinuria/Homocysteinemia Fabry Disease MELAS Syndrome Hyperglycemia and Hypoglycemia in 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.)
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Noncontrast computed tomography (CT) scan in a 52-year-old man
with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity
and sulcal effacement with mass effect involving the left anterior and middle cerebral artery
territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity
noted suggestive of developing petechial hemorrhage in this large area of infarction.
Magnetic resonance angiogram (MRA) in a 52-year-old man
demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red
circle), occlusion or high-grade stenosis of the distal middle cerebral artery (MCA) trunk and
attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high
signal confirmed to be true restricted diffusion on the apparent diffusion coefficient (ADC) map
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consistent with acute infarction. Maximum intensity projection (MIP)
image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-
grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle),
suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis
and occlusions, which account for approximately one third of ischemic strokes.Lacunar strokes
Lacunar strokes represent 13-20% of all ischemic strokes. They result from occlusion of the
penetrating branches of the MCA, the lenticulostriate arteries, or the penetrating branches of the
circle of Willis, vertebral artery, or basilar artery. The great majority of lacunar strokes are
related to hypertension. (See the image below.)
Axial noncontrast computed tomography (CT) scan demonstrates
a focal area of hypodensity in the left posterior limb of the internal capsule in a 60-year-old man
with acute onset of right-sided weakness. The lesion demonstrates high signal on the fluid-
attenuated inversion recovery (FLAIR) sequence (middle image) and diffusion-weighted
magnetic resonance imaging (MRI) scan (right image), with low signal on the apparent diffusion
coefficient (ADC) maps indicating an acute lacunar infarction. Lacunar infarcts are typically no
more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata,
brainstem, and cerebellum.
Causes of lacunar infarcts include the following:
Microatheroma Lipohyalinosis
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Fibrinoid necrosis secondary to hypertension or vasculitis Hyaline arteriosclerosis Amyloid angiopathy Microemboli
Embolic strokes
Cardiogenic emboli may account for up to 20% of acute strokes. Emboli may arise from the
heart, the extracranial arteries, including the aortic arch or, rarely, the right-sided circulation
(paradoxical emboli) with subsequent passage through a patent foramen ovale.[36] Sources of
cardiogenic emboli include the following:
Valvular thrombi (eg, inmitral stenosis orendocarditis or from use of a prosthetic valve) Mural thrombi (eg, inmyocardial infarction,atrial fibrillation, dilated cardiomyopathy, or
severe congestive heart failure)
Atrial myxomaAcute myocardial infarction is associated with a 2-3% incidence of embolic strokes, of which
85% occur in the first month after the infarction.[37] Embolic strokes tend to have a sudden onset,
and neuroimaging may demonstrate previous infarcts in several vascular territories or may show
calcific emboli.
Cardioembolic strokes may be isolated, multiple and in a single hemisphere, or scattered and
bilateral; the latter 2 types indicate multiple vascular distributions and are more specific for
cardioembolism. Multiple and bilateral infarcts can be the result of embolic showers or recurrent
emboli. Other possibilities for single and bilateral hemispheric infarctions include emboli
originating from the aortic arch and diffuse thrombotic or inflammatory processes that can lead
to multiple small-vessel occlusions. (See the image below.)[38, 39]
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
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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, seeCardioembolic Stroke.
Thrombotic strokes
Thrombogenic factors may include injury to and loss of endothelial cells; this loss exposes the
subendothelium and results in 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 promote 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 of thrombotic stroke in patients with widespread
atherosclerosis. In other patients, especially younger patients, other causes should be considered,
including the following[8, 40] :
Hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein Sdeficiency, pregnancy)
Sickle cell disease Fibromuscular dysplasia Arterial dissections Vasoconstriction associated with substance abuse (eg, cocaine, amphetamines)
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 to severe
hypoperfusion, as occurs, for example, in carotid occlusion or prolonged hypotension. (See the
image below.)[41, 42, 43]
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Magnetic resonance imaging (MRI) scan was obtained in a 62-
year-old man with hypertension and diabetes and a history of transient episodes of right-sided
weakness and aphasia. The fluid-attenuated inversion recovery (FLAIR) image (left)
demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter,
bilaterally. This configuration is typical for deep border-zone, or watershed, infarction, in this
case the anterior and posterior middle cerebral artery (MCA) watershed areas. The left-sided
infarcts have corresponding low signal on the apparent diffusion coefficient (ADC) map (right),signifying acuity. An old left posterior parietal infarct is noted as well.
Flow disturbances
Stroke symptoms can result from inadequate cerebral blood flow because of decreased blood
pressure (and specifically, decreased cerebral perfusion pressure) or as a result of hematologic
hyperviscosity from 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, seeBlood Dyscrasias and Stroke.
Epidemiology
Stroke is the leading cause of disability and the fourth leading cause of death in the United
States.[44, 45] Each year, approximately 795,000 people in the United States experience new
(610,000 people) or recurrent (185,000 people) stroke.[6]Epidemiologic studies indicate that 82-
92% of strokes in the United States are ischemic.
According to the World Health Organization (WHO), 15 million people suffer stroke worldwide
each year. Of these, 5 million die, and another 5 million are left permanently disabled.[46]
Race-, sex-, and age-related demographics
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In the United States, blacks have an age-adjusted risk of death from stroke that is 1.49 times that
of whites.[47] 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 men 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%.
Although stroke often is considered a disease of elderly persons, one third of strokes occur in
persons younger than 65 years.[45] Risk of stroke increases with age, especially in patients older
than 64 years, in whom 75% of all strokes occur.
Prognosis
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%. However, the prognosis after acute ischemic
stroke varies greatly in individual patients, depending on the stroke severity and on the patients
premorbid condition, age, and poststroke complications.[4]
A study utilizing the large national Get With The Guidelines - Stroke registry found that the
baseline National Institutes of Health Stroke Scale (NIHSS) score was the strongest predictor of
early mortality risk, even more so than currently used mortality prediction models incorporating
multiple clinical data.[48] Cardiogenic emboli are associated with the highest 1-month mortality in
patients with acute stroke.
The presence of computed tomography (CT) scan evidence of infarction early in presentation has
been associated with poor outcome and with an increased propensity for hemorrhagic
transformation after fibrinolytic therapy (see Pathophysiology).
[5, 49, 50]
Hemorrhagictransformation is estimated to occur in 5% of uncomplicated ischemic strokes in the absence of
fibrinolytic therapy, although it is not always associated with neurologic decline. Indeed,
hemorrhagic transformation ranges from the development of small petechial hemorrhages to the
formation of hematomas requiring evacuation.
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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
fibrinolysis, as well as extension of the infarcted territory.[51, 52, 53]
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. For more information, see the Medscape Reference articleMotor Recovery in Stroke.
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 could include local churches, employers,
and senior organizations to promote stroke awareness.
The American Stroke Association (ASA) advises the public to be aware of the symptoms of
stroke that are easily recognized, including the sudden onset of any of the following, and to call
911 immediately:
Numbness or weakness of face, arm, or leg, especially on 1 side of the body
Confusion Difficulty in speaking or understanding Deterioration of vision in 1 or both eyes Difficulty in walking, dizziness, and loss of balance or coordination Severe headache with no known cause
In the spring of 2013, the ASA launched a stroke public education campaign that uses the
acronymFAST to teach the warning signs of stroke and the importance of calling 911, asfollows:
F: Face drooping A: Arm weakness S: Speech difficulty
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T: Time to call 911
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BAB II PRESENTATION
History
A focused medical history for patients with ischemic stroke aims to identify risk factors for
atherosclerotic and cardiac disease, including the following (see Etiology):
Hypertension Diabetes mellitus Tobacco use High cholesterol History of coronary artery disease, coronary artery bypass, or atrial fibrillation
In younger patients, elicit a history of the following:
Recent trauma Coagulopathies Illicit drug use (especially cocaine) Migraines Oral contraceptive use
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 fromhemorrhagic stroke, although nausea, vomiting, headache, and a sudden change in the patients
level of consciousness are more common in hemorrhagic strokes.
Consider stroke in any patient presenting with acute neurologic deficit or any alteration in level
of consciousness. Common signs and symptoms of stroke include the abrupt onset of any of the
following:
Hemiparesis, monoparesis, or (rarely) quadriparesis Hemisensory deficits Monocular or binocular visual loss Visual field deficits Diplopia Dysarthria
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Facial droop Ataxia Vertigo (rarely in isolation) Aphasia Sudden decrease in the level of consciousness
Although such symptoms can occur alone, they are more likely to occur in combination.
Establishing the time at which the patient was last without stroke symptoms, or last known to be
normal, is especially critical when fibrinolytic therapy is an option. Unfortunately, the median
time from symptom onset to emergency department (ED) presentation ranges from 4-24 hours in
the United States.[3]
Multiple factors contribute to delays in seeking care for symptoms of stroke. Many strokes occur
while patients are sleeping and are not discovered until the patient wakes (this phenomenon is
also known as "wake-up" stroke). Stroke can leave some patients too incapacitated to call for
help. Occasionally, a stroke goes unrecognized by patients or their caregivers.[6, 54]
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. Input from 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 are as follows:
Detect extracranial causes of stroke symptoms Distinguish stroke from stroke mimics
Determine and document for future comparison the degree of deficit Localize the lesion Identify comorbidities Identify conditions that may influence treatment decisions (eg, trauma, active bleeding, active
infection)
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The physical examination always includes a careful head and neck examination for signs of
trauma, infection, and meningeal irritation. A careful search for the cardiovascular causes of
stroke requires examination of the following:
Ocular fundi (retinopathy, emboli, hemorrhage) Heart (irregular rhythm, murmur, gallop) Peripheral vasculature (palpation of carotid, radial, and femoral pulses; auscultation for carotid
bruit)
The physical examination must encompass all of the major organ systems, starting with airway,
breathing, and circulation (ABCs) and the vital signs. Patients with a decreased level of
consciousness should be assessed to ensure that they are able to protect their airway. Patients
with stroke, especially hemorrhagic stroke, can suffer quick clinical deterioration; 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.
Head and neck, cardiac, and extremities 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 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 heart failure; thus, auscultation for murmurs and gallops is
recommended.
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Carotid or vertebrobasilar dissections and, less commonly, thoracic aortic dissections may cause
ischemic stroke. Unequal pulses or blood pressures in the extremities may reflect the presence of
aortic dissections.
Neurologic examination
With the availability of fibrinolytic 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 the neurologic examination include the following:
Confirming the presence of a stroke syndrome (to be defined further with cranial CT scanning) Distinguishing stroke from stroke mimics Establishing a neurologic baseline should the patient's condition improve or deteriorate Establishing stroke severity to assist in prognosis and therapeutic selection
Essential components of the neurologic examination include the following evaluations:
Cranial nerves Motor function Sensory function Cerebellar function Gait Deep tendon reflexes Language (expressive and receptive capabilities) Mental status and level of consciousness
The skull and spine also should be examined, and signs of meningismus should be sought.
National Institutes of Health Stroke Scale
A useful tool in quantifying neurologic impairment is the National Institutes of Health StrokeScale (NIHSS) (see Table 2, below). The NIHSS enables the healthcare provider to rapidly
determine the severity and possible location of the stroke. NIHSS scores are strongly associated
with outcome and can help to identify those patients who are likely to benefit from fibrinolytic
therapy and those who are at higher risk of developing hemorrhagic complications of fibrinolytic
use.
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The NIHSS is easily performed; it focuses on the following 6 major areas of the neurologic
examination:
level of consciousness Visual function Motor function Sensation and neglect Cerebellar function Language
The NIHSS is a 42-point scale. Patients with minor strokes usually have a score of less than 5.
An NIHSS score of greater than 10 correlates with an 80% likelihood of proximal vessel
occlusions (as identified on CT or standard angiograms). However, discretion must be used inassessing the magnitude of the clinical deficit and resulting disability; for instance, if a patient's
only deficit is mutism, the NIHSS score will be 3. Additionally, the scale does not measure some
deficits associated with posterior circulation strokes (ie, vertigo, ataxia).[55]
Table 2. National Institutes of Health Stroke Scale(Open Table in a new window)
Category Description Score
1a level of consciousness (LOC) Alert
Drowsy
Stuporous
0
1
2
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Coma 3
1b LOC questions (month, age) Answers both correctly
Answers 1 correctly
Incorrect on both
0
1
2
1c LOC commands (open and close eyes,
grip and release nonparetic hand)
Obeys both correctly
Obeys 1 correctly
Incorrect on both
0
1
2
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2 Best gaze (follow finger) Normal
Partial gaze palsy
Forced deviation
0
1
2
3 Best visual (visual fields) No visual loss
Partial hemianopia
Complete hemianopia
Bilateral hemianopia
0
1
2
3
4 Facial palsy (show teeth, raise brows, Normal 0
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squeeze eyes shut) Minor
Partial
Complete
1
2
3
5 Motor arm left* (raise 90, hold 10 seconds) No drift
Drift
Cannot resist gravity
No effort against gravity
0
1
2
3
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No movement 4
6 Motor arm right* (raise 90, hold 10 seconds) No drift
Drift
Cannot resist gravity
No effort against gravity
No movement
0
1
2
3
4
7 Motor leg left* (raise 30, hold 5 seconds) No drift
Drift
0
1
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Cannot resist gravity
No effort against gravity
No movement
2
3
4
8 Motor leg right* (raise 30, hold 5 seconds) No drift
Drift
Cannot resist gravity
No effort against gravity
0
1
2
3
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No movement 4
9 Limb ataxia (finger-nose, heel-shin) Absent
Present in 1 limb
Present in 2 limbs
0
1
2
10 Sensory (pinprick to face, arm, leg) Normal
Partial loss
Severe loss
0
1
2
11 Extinction/neglect (double simultaneous No neglect 0
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testing)
Partial neglect
Complete neglect
1
2
12 Dysarthria (speech clarity to "mama,
baseball, huckleberry, tip-top, fifty-fifty")
Normal articulation
Mild to moderate dysarthria
Near to unintelligible or worse
0
1
2
13 Best language** (name items,
describe pictures)
No aphasia
Mild to moderate aphasia
0
1
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Severe aphasia
Mute
2
3
Total - 0-42
* For limbs with amputation, joint fusion, etc, score 9 and explain.
** For intubation or other physical barriers to speech, score 9 and explain. Do not add 9 to the
total score.NIH Stroke Scale (PDF)
Middle cerebral artery stroke
Middle cerebral artery (MCA) occlusions commonly produce the following:
Contralateral hemiparesis Contralateral hypesthesia Ipsilateral hemianopsia Gaze preference toward the side of the lesion Agnosia Receptive or expressive aphasia, if the lesion occurs in the dominant hemisphere
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Neglect, inattention, and extinction of double simultaneous stimulation, with somenondominant hemisphere lesions
The MCA supplies the upper extremity motor strip. Consequently, weakness of the arm and face
is usually worse than that of the lower limb.
Anterior cerebral artery stroke
Anterior cerebral artery (ACA) occlusions primarily affect frontal lobe function. Findings in
ACA stroke may include the following:
Disinhibition and speech perseveration Primitive reflexes (eg, grasping, sucking reflexes) Altered mental status Impaired judgment Contralateral weakness (greater in legs than arms) Contralateral cortical sensory deficits Gait apraxia Urinary incontinence
Posterior cerebral artery stroke
Posterior cerebral artery (PCA) occlusions affect vision and thought. Manifestations include the
following:
Contralateral homonymous hemianopsia Cortical blindness Visual agnosia Altered mental status Impaired memory
Vertebrobasilar artery occlusions are particularly difficult to localize, because they may cause a
wide variety of cranial nerve, cerebellar, and brainstem deficits. These include the following:
Vertigo Nystagmus Diplopia
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Visual field deficits Dysphagia Dysarthria Facial hypesthesia Syncope Ataxia
A hallmark of posterior circulation stroke is the presence of crossed findings: ipsilateral cranial
nerve deficits and contralateral motor deficits. This contrasts with 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.
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BAB III
Diagnostic Considerations
Stroke mimics commonly confound the clinical diagnosis of stroke. One study reported that 19%
of patients diagnosed with acute ischemic stroke by neurologists before cranial CT scanning
actually had non-cerebrovascular causes for their symptoms.
The most frequent stroke mimics include the following:
Seizure (17%) Systemic infection (17%) Brain tumor (15%) Toxic-metabolic disorders, such as hyponatremia and hypoglycemia (13%) Positional vertigo (6%) Conversion disorder
In the prehospital and emergency department (ED) settings, hypoglycemia is a common stroke
mimic and is particularly important to consider, since it can be readily detected and corrected.[56,
57] For more information, seeHyperglycemia and Hypoglycemia in Stroke.
Ischemic versus hemorrhagic stroke
Although the definitive distinction of ischemic stroke from hemorrhagic stroke requires
neuroimaging, a meta-analysis found that the following clinical findings increase the probability
of hemorrhagic stroke[58] :
Coma (likelihood ratio [LR] 6.2) Neck stiffness (LR 5.0) Seizures accompanying the neurologic deficit (LR, 4.7) Diastolic blood pressure >110 mm Hg (LR, 4.3) Vomiting (LR, 3.0)
Findings that decrease the probability of hemorrhage include cervical bruit (LR 0.12) and prior
transient ischemic attack (LR, 0.34).
Transient ischemic attack
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Transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction that
results from focal cerebral, spinal cord, or retinal ischemia and is not associated with acute tissue
infarction. Roughly 80% of TIAs resolve within 60 minutes.[59] TIA can result from the same
mechanisms as ischemic stroke. Data suggest that roughly 10% of patients with TIA suffer
stroke within 90 days and of those, half suffer stroke within 2 days.[60, 61]
The classic definition of TIA included symptoms lasting as long as 24 hours. With advances in
neuroimaging, however, it now appears that many such cases represent minor strokes with
resolved symptoms rather than true TIAs. Thus, the current definition of TIA is based on tissue
pathophysiology rather than symptom duration.[59]
Cerebral venous thrombosis
Diagnosis and management of a rare form of stroke,cerebral venous thrombosis (CVT), was the
subject of a 2011 American Heart Association/American Stroke Association (AHA/ASA)
statement for healthcare professionals. According to the statement, diagnosing CVT requires a
high degree of clinical suspicion. Most people diagnosed with CVT present with headache, often
of increasing severity and usually accompanied by focal neurologic signs.[48]
Differentials
Bell Palsy
Brain Neoplasms
Conversion Disorder in Emergency Medicine
Hemorrhagic Stroke
Hypoglycemia
Migraine Headache
Seizure Assessment in the Emergency Department
Emergent Management of Subarachnoid Hemorrhage
http://emedicine.medscape.com/article/1910519-overviewhttp://emedicine.medscape.com/article/1162804-overviewhttp://emedicine.medscape.com/article/1146903-overviewhttp://emedicine.medscape.com/article/779664-overviewhttp://emedicine.medscape.com/article/805361-overviewhttp://emedicine.medscape.com/article/1916662-overviewhttp://emedicine.medscape.com/article/122122-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/1609294-overviewhttp://emedicine.medscape.com/article/794076-overviewhttp://emedicine.medscape.com/article/794076-overviewhttp://emedicine.medscape.com/article/1609294-overviewhttp://emedicine.medscape.com/article/1142556-overviewhttp://emedicine.medscape.com/article/122122-overviewhttp://emedicine.medscape.com/article/1916662-overviewhttp://emedicine.medscape.com/article/805361-overviewhttp://emedicine.medscape.com/article/779664-overviewhttp://emedicine.medscape.com/article/1146903-overviewhttp://emedicine.medscape.com/article/1162804-overviewhttp://emedicine.medscape.com/article/1910519-overview -
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Syncope
Transient Global Amnesia
Bells palsy
Practice Essentials
Bell palsy, also termed idiopathic facial paralysis (IFP), is the most common cause of unilateral
facial paralysis and the most common cause of facial paralysis worldwide. It is one of the most
common neurologic disorders of the cranial nerves. In the great majority of cases, Bell palsy
gradually resolves over time, and its cause is unknown.
Essential update: New Bell palsy guidelines issued by the The American Academy of
OtolaryngologyHead and Neck Surgery Foundation
The American Academy of OtolaryngologyHead and Neck Surgery Foundation has issued
updated guidelines for the diagnosis and management of Bell palsy that recommend the use of
corticosteroids within 72 hours after the onset of symptoms in patients 16 years of age and older.
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Antiviral agents (eg, acyclovir, valacyclovir) may be considered if a viral etiology is suspected,
but only in combination with corticosteroids.[1]
Additional recommendations include the following[1] :
Patients with acute-onset unilateral facial paralysis should be assessed to exclude otherpossible identifiable causes (eg, herpes zoster, Lyme disease, sarcoidosis)
Diagnostic imaging and routine lab testing are not recommended for patients with new-onsetdisease
Electrodiagnostic testing is not recommended in patients with incomplete facial paralysis;however, it may be offered to those patients with complete facial paralysis
If there is impaired eye closure, appropriate eye protection should be implemented Referral to a facial nerve specialist should occur in cases of new or worsening neurologic
symptoms, developing ocular symptoms, or incomplete facial recovery after 3 months
These guidelines concur with the American Academy of Neurology guidelines issued in 2012.[2]
Signs and symptoms
Signs and symptoms of Bell palsy include the following:
Acute onset of unilateral upper and lower facial paralysis (over a 48-hr period)
Posterior auricular pain Decreased tearing Hyperacusis Taste disturbances Otalgia Weakness of the facial muscles Poor eyelid closure Aching of the ear or mastoid Tingling or numbness of the cheek/mouth Epiphora Ocular pain Blurred vision Flattening of forehead and nasolabial fold on the side affected by palsy
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When patient raises eyebrows, palsy-affected side of forehead remains flat When patient smiles, face becomes distorted and lateralizes to side opposite the palsySeeClinical Presentation for more specific information on the signs and symptoms of Bell palsy.
Diagnosis
Examination for Bell palsy includes the following:
Otologic examination: Pneumatic otoscopy and tuning fork examination, particularly ifevidence of acute or chronic otitis media
Ocular examination: Patient often unable to completely close eye on affected side Oral examination: Taste and salivation often affected Neurologic examination: All cranial nerves, sensory and motor testing, cerebellar testingGrading
The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to
VI,[3, 4, 5] as follows:
Grade I: normal facial function
Grade II: mild dysfunction
Grade III: moderate dysfunction
Grade IV: moderately severe dysfunction
Grade V: severe dysfunction
Grade VI: total paralysis
SeeClinical Presentation for more specific information on patient history and physical
examination for Bell palsy.
Testing
Although there are no specific diagnostic tests for Bell palsy, the following may be useful for
identifying or excluding other disorders:
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Rapid plasma reagin and/or venereal disease research laboratory test or fluorescenttreponemal antibody absorption test
HIV screening by enzyme-linked immunosorbent assay and/or Western blot Complete blood count Erythrocyte sedimentation rate Thyroid function Serum glucose CSF analysis Blood glucose Hemoglobin A1c Antineutrophil cytoplasmic antibody levels Salivary flow Schirmer blotting test Nerve excitability test Computed tomography Magnetic resonance imagingSeeWorkup for more specific information on testing and imaging modalities for Bell palsy.
Management
Goals of treatment: (1) improve facial nerve (seventh cranial nerve) function; (2) reduce
neuronal damage; (3) prevent complications from corneal exposure
Treatment includes the following:
Corticosteroid therapy (prednisone)[6, 7] Antiviral agents[6, 8] Eye care: Topical ocular lubrication is usually sufficient in most cases to prevent corneal
drying, abrasion, and ulcers[9]
Surgical options
Surgical treatment options include the following:
Facial nerve decompression Subocularis oculi fat lift
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Implantable devices (eg, gold weights) placed into the eyelid Tarsorrhaphy Transposition of the temporalis muscle Facial nerve grafting Direct brow liftSeeTreatment andMedication for more specific information regarding pharmacologic and other
therapies for Bell palsy.
Image library
Left-sided Bell palsy.
Background
Bell palsy, more appropriately termed idiopathic facial paralysis (IFP), is the most common
cause of unilateral facial paralysis. Bell palsy is an acute, unilateral, peripheral, lower-motor-
neuronfacial nerve paralysis that gradually resolves over time in 80-90% of cases.
Controversy surrounds the etiology and treatment of Bell palsy. The cause of Bell palsy remains
unknown, though the disorder appears to be a polyneuritis with possible viral, inflammatory,
autoimmune, and ischemic etiologies. Increasing evidence implicates herpes simplex type I and
herpes zoster virus reactivation from cranial-nerve ganglia.[10] (See Etiology.)
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Bell palsy is one of the most common neurologic disorders affecting the cranial nerves, and it is
the most common cause of facial paralysis worldwide. It is thought to account for approximately
60-75% of cases of acute unilateral facial paralysis. Bell palsy is more common in adults, in
people with diabetes, and in pregnant women. (See Epidemiology.)
Diagnosis
Determining whether facial nerve paralysis is peripheral or central is a key step in the diagnosis.
A lesion involving the central motor neurons above the level of the facial nucleus in the pons
causes weakness of the lower face alone. Thorough history taking and examination, including the
ears, nose, throat, and cranial nerves, must be performed. (See Presentation.)
The minimum diagnostic criteria include paralysis or paresis of all muscle groups on one side of
the face, sudden onset, and absence of central nervous system (CNS) disease. Note that the
diagnosis of IFP can be made only after other causes of acute peripheral palsy have been
excluded. (See DDx.)
If the clinical findings are doubtful or if paralysis lasts longer than 6-8 weeks, further
investigations, including gadolinium-enhanced magnetic resonance imaging (MRI) of the
temporal bones and pons, should be considered.[11] Electrodiagnostic tests (eg, stapedius reflex
test, evokedfacial nerve electromyography [EMG], audiography) may help to improve the
accuracy of prognosis in difficult cases. (See Workup.)
Treatment
Treatment of Bell palsy should be conservative and guided by the severity and probable
prognosis in each particular case. Studies have shown the benefit of high-dose corticosteroids for
acute cases.[12, 13] Although antiviral treatment has also come into use, evidence is now available
indicating that it may not be beneficial.[12] (See Treatment and Medication.)
Topical ocular therapy is useful in most cases, with the exception of those in which the condition
is severe or prolonged. In these cases, surgical management is best. Several procedures are aimed
at protecting the cornea from exposure and achieving facial symmetry. These procedures reduce
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the need for constant use of lubrication drops or ointments, may improve cosmesis, and may be
needed to preserve vision on the affected side. (See Treatment.)
Patient education
To prevent corneal abrasions, patients should be instructed about eye care. They also should be
encouraged to do facial muscle exercises using passive range of motion, as well as actively close
their eyes and smile.
For patient education information, see theBrain and Nervous System Center,as well asBells
Palsy.
Anatomy
In 1550, Fallopius noted the narrow foramen in the temporal bone through which a part of theseventh cranial nerve (facial nerve) passes; this feature is now sometimes called the fallopian
canal or the facial canal. In 1828, Charles Bell made the distinction between the fifth and seventh
cranial nerves; he noted that the seventh nerve was involved mainly in the motor function of the
face and that the fifth nerve primarily conducted sensation from the face.
The facial nerve contains parasympathetic fibers to the nose, palate, and lacrimal glands. Its
course is tortuous, both centrally and peripherally. The facial nerve travels a 30-mm intraosseous
course through the internal auditory canal (with the eighth cranial nerve) and through the internal
fallopian canal in the petrous temporal bone. This bony confinement limits the amount that the
nerve can swell before it becomes compressed.
The nucleus of the facial nerve lies within the reticular formation of the pons, adjacent to the
fourth ventricle. The facial nerve roots include fibers from the motor, solitary, and salivatory
nuclei. The preganglionic parasympathetic fibers that originate in the salivatory nucleus join the
fibers from nucleus solitarius to form the nervus intermedius.
The nervus intermedius is composed of sensory fibers from the tongue, mucosa, and
postauricular skin, as well as parasympathetic fibers to the salivary and lacrimal glands. These
fibers then synapse with the submandibular ganglion, which has fibers that supply the sublingual
and submandibular glands. The fibers from the nervus intermedius also supply the
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pterygopalatine ganglion, which has parasympathetic fibers that supply the nose, palate, and
lacrimal glands.
The fibers of the facial nerve then course around the sixth cranial nerve nucleus and exit the pons
at the cerebellopontine angle. The fibers go through the internal auditory canal along with thevestibular portion of the eighth cranial nerve.
The facial nerve passes through the stylomastoid foramen in the skull and terminates into the
zygomatic, buccal, mandibular, and cervical branches. These nerves serve the muscles of facial
expression, which include the frontalis, orbicularis oculi, orbicularis oris, buccinator, and
platysma muscles. Other muscles innervated by the facial nerve include the stapedius,
stylohyoid, posterior belly of the digastric, occipitalis, and anterior and posterior auricular
muscles. All muscles innervated by the facial nerve are derived from the second branchial arch.
See the images below.
The facial nerve.
Pathophysiology
The precise pathophysiology of Bell palsy remains an area of debate. The facial nerve courses
through a portion of the temporal bone commonly referred to as the facial canal. A populartheory proposes that edema and ischemia result in compression of the facial nerve within this
bony canal. The cause of the edema and ischemia has not yet been established. This compression
has been seen in MRI scans with facial nerve enhancement.[14]
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The first portion of the facial canal, the labyrinthine segment, is the narrowest; the meatal
foramen in this segment has a diameter of only about 0.66 mm. This is the location that is
thought to be the most common site of compression of the facial nerve in Bell palsy. Given the
tight confines of the facial canal, it seems logical that inflammatory, demyelinating, ischemic, or
compressive processes may impair neural conduction at this site.
Injury to the facial nerve in Bell palsy is peripheral to the nerves nucleus. The injury is thought
to occur near, or at, the geniculate ganglion. If the lesion is proximal to the geniculate ganglion,
the motor paralysis is accompanied by gustatory and autonomic abnormalities. Lesions between
the geniculate ganglion and the origin of the chorda tympani produce the same effect, except that
they spare lacrimation. If the lesion is at the stylomastoid foramen, it may result in facial
paralysis only.
Etiology
Herpes simplex virus
In the past, situations that produced cold exposure (eg, chilly wind, cold air conditioning, or
driving with the car window down) were considered to be the only triggers for Bell palsy.
Several authors now believe, however, that the herpes simplex virus (HSV) is a common cause
of Bell palsy, though a definitive causal relationship of HSV to Bell palsy may be difficult to
prove because of the ubiquitous nature of HSV.
The hypothesis that HSV is the etiologic agent in Bell palsy holds that after causing primary
infection on the lips (ie, cold sores), the virus travels up the axons of the sensory nerves and
resides in the geniculate ganglion. At times of stress, the virus reactivates and causes local
damage to the myelin.
This hypothesis was first suggested in 1972 by McCormick.[15] Autopsy studies have since
shown HSV in the geniculate ganglion of patients with Bell palsy. Murakami et al performed
polymerase chain reaction (PCR) assay testing on the endoneural fluid of the facial nerve in
patients who underwentsurgery for Bell palsy and found HSV in 11 of 14 cases.[16]
Additional support for a viral etiology was seen when intranasal, inactivated influenza vaccine
was strongly linked to the development of Bell palsy.[17, 18] With those cases, however, it is not
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clear whether another component of the vaccine caused the paresis, which was then accompanied
by a reactivation of HSV infection.
Additional causes
Besides HSV infection, possible etiologies for Bell palsy include other infections (eg, herpes
zoster, Lyme disease, syphilis, Epstein-Barr viral infection, cytomegalovirus, human
immunodeficiency virus [HIV], mycoplasma); inflammation alone; and microvascular disease
(diabetes mellitus and hypertension). Bell palsy has also been known to follow recent upper
respiratory infection (URI).[19, 20, 21, 22, 23, 24]
Bell palsy may be secondary to viral and/or autoimmune reactions that cause the facial nerve to
demyelinate, resulting in unilateral facial paralysis.
A family history of Bell palsy has been reported in approximately 4% of cases. Inheritance in
such cases may be autosomal dominant with low penetration; however, which predisposing
factors are inherited is unclear.[25] The family history may also be positive for other nerve, nerve
root, or plexus disorders (eg, trigeminal neuralgia) in siblings.[26] In addition, there are isolated
reports of familial Bell palsy with neurologic deficits, including ophthalmoplegia[27] and essential
tremor.[28] A rare form of familial Bell palsy has a predilection for juvenile females.[29]
Because there is a strong environmental predisposition to Bell palsy, due to the common viraletiology, a positive family history may or may not indicate a true genetic etiology.
Epidemiology
In the United States, the annual incidence of Bell palsy is approximately 23 cases per 100,000
persons.[7] Very few cases are observed during the summer months. Internationally, the highest
incidence was found in a study in Seckori, Japan, in 1986, and the lowest incidence was found in
Sweden in 1971. Most population studies generally show an annual incidence of 15-30 cases per
100,000 population.
Bell palsy is thought to account for approximately 60-75% of cases of acute unilateral facial
paralysis, with the right side affected 63% of the time. It can also be recurrent, with a reported
recurrence range of 4-14%.[20]
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Though bilateral simultaneous Bell palsy can develop, it is rare. It accounts for only 23% of
bilateral facial paralysis and has an occurrence rate that is less than 1% of that for unilateral
facial nerve palsy.[30, 31] The majority of patients with bilateral facial palsy have Guillain-Barr
syndrome, sarcoidosis, Lyme disease, meningitis (neoplastic or infectious), or bilateral
neurofibromas (in patients with neurofibromatosis type 2).
Persons with diabetes have a 29% higher risk of being affected by Bell palsy than do persons
without diabetes. Thus, measuring blood glucose levels at the time of diagnosis of Bell palsy
may detect undiagnosed diabetes. Diabetic patients are 30% more likely than nondiabetic
patients to have only partial recovery; recurrence of Bell palsy is also more common among
diabetic patients.[32]
Bell palsy is also more common in people who are immunocompromised or in women with
preeclampsia.[33]
Sex- and age-related demographics
Bell palsy appears to affect the sexes equally. However, young women aged 10-19 years are
more likely to be affected than are men in the same age group. Pregnant w