Practice Essentials

Ischemic stroke (see the image below) 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.

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.
See Acute Stroke, a Critical Images slideshow, for more information on incidence, presentation,
intervention, and additional resources.

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
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 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.

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 angiography

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

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 or anticoagulants
are to be used
Cardiac biomarkers: Important because of the association of cerebral vascular disease and
coronary artery disease
Toxicology screening: May assist in identifying intoxicated patients with symptoms/behavior
mimicking stroke syndromes
Pregnancy testing: A urine pregnancy test should be obtained for all women of childbearing age
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 gas
defines the severity of hypoxemia and may be used to detect acid-base disturbances
See Workup for more detail.

Management
The goal for the emergent management of stroke is to complete the following within 60 minutes of patient
arrival[1] :
 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 [2, 3]
Mechanical thrombectomy
Treatment of comorbid conditions may include the following:

Reduce fever
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

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 membrane and cell depolarization. Influx of
sodium and calcium ions and passive inflow of water into the cell lead to cytotoxic edema. [7, 8, 9]

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. [10]
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.[10]

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, 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 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.[11] 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.[12, 13]

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. [11] 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.)
 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 emboli.
 Vascular distributions: Posterior cerebral
artery (PCA) infarction. The noncontrast computed tomography (CT) images demonstrate PCA distribution infarction
involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional
involvement of the thalamus, also part of the PCA territory.

Vascular distributions: Anterior choroidal

artery 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 cerebral artery
(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 evacuation or 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 barrier, red blood cells extravasate
from the weakened capillary bed, producing petechial hemorrhage or more frank intraparenchymal
hematoma.[7, 14, 15]

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.[3, 7, 16]Hemorrhagic transformation is also more likely following administration of rt-PA in
patients whose noncontrast CT (NCCT) scans demonstrate areas of hypodensity.[17, 18, 19]

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%).[1] 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 ischemic stroke. [1] 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. 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 (although there are likely many others):

Age
Race
Sex
Ethnicity
History of migraine headaches [20]
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
In 2014, the American Heart Association and the American Stroke Association issued guidelines for the
reduction of stroke risk specifically in women. These gender-specific recommendations include the
following[24, 25] :

A stroke risk score should be developed specifically for women

 Women with a history of high blood pressure before pregnancy should be considered for low-dose
aspirin and/or calcium supplement treatment to reduce the risk of preeclampsia
Blood pressure medication may be considered for pregnant women with moderately high blood
pressure (150-159 mmHg/100-109 mmHg), and pregnant women with severe high blood pressure
(160/110 mmHg or above) should be treated
Women should be screened for high blood pressure before they start using birth control pills
because of an increased risk of stroke
Women with migraine headaches with aura should be encouraged to quit smoking to reduce the
risk of stroke
Women over age 75 should be screened for atrial fibrillation
Genetic and inflammatory mechanisms
Evidence continues to accumulate that inflammation and genetic factors have important roles in the
development 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) 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 disorders with 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

the F2 and F5 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 [26]

ALOX5AP: Involved in the metabolism of arachidonic acid [27]

PRKCH: Involved in major signal transduction systems [28]
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
for MTHFR mutation, 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 recessive manner.
Symptoms usually manifest early in life. Patients have a marfanoid habitus, ectopia lentis, and myopia and
generally have intellectual disability.[29]

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.[30] 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 CST3 gene
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.[31]

CADASIL

Cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy (CADASIL),
is caused by mutations in the NOTCH3 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. [32]

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.[33]

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.[34]

Large-vessel stroke has been associated with variations in HDAC9, PITX2, andZFHX3.[35] HDAC9 is located
on7p21.1, while PITX2 and ZFHX3 are 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.[36] An additional study suggested an association between ischemic stroke and
a locus on 12p13.[37]

For more information, see Genetic 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.)

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 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
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.[38] Sources of cardiogenic emboli include the
following:

Valvular thrombi (eg, in mitral stenosis or endocarditis or from use of a prosthetic valve)
Mural thrombi (eg, in myocardial infarction, atrial fibrillation, dilated cardiomyopathy, or severe
congestive heart failure)
Atrial myxoma
Acute myocardial infarction is associated with a 2-3% incidence of embolic strokes, of which 85% occur in
the first month after the infarction.[39] 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.) [40, 41]

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; 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[7, 42] :

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

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.) [43, 44, 45]

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, see Blood Dyscrasias and Stroke.