Neurology

Lecture 11
by
Selen Gür Özmen MD PhD
Neurologist
Neuroscientist

Aminoff Clinical Neurology 9th

Version
Stroke Chapter 13
• Stroke is the fourth leading cause of death in
the United States (after heart disease, cancer,
and chronic lung disease) and the most
common disabling neurologic disorder.
• Approximately 800,000 new strokes occur and
approximately 130,000 people die from stroke
in the United States each year.
• The incidence of stroke increases with age, with
approximately two-thirds of all strokes occurring
in those older than 65 years.
• Age-adjusted stroke risk is somewhat higher in
men than in women.
• Modifiable risk factors for stroke include;
– systolic or diastolic hypertension
– atrial fibrillation
– diabetes
– dyslipidemia
– physical inactivity
• The incidence of stroke has decreased in recent
decades, largely because of improved
treatment of hypertension, dyslipidemia, and
diabetes, and reduction in smoking.
• Genetic factors also appear to be important in
stroke pathogenesis, although the cause of
most strokes is likely to be multifactorial and
involve both polygenic and environmental
influences.
 APPROACH TO DIAGNOSIS

• Stroke is a syndrome characterized by four key

features:
• 1. Sudden onset—The sudden onset of
symptoms is documented by the history.
• 2. Focal involvement of the central nervous
system— The site of involvement is suggested by
the symptoms and signs, delineated more
precisely by neurologic examination, and
confirmed by imaging studies (computed
tomography [CT] or magnetic resonance imaging
[MRI]).
 APPROACH TO DIAGNOSIS

• 3. Lack of rapid resolution—The duration of

neurologic deficits is documented by the history.
• The classic definition of stroke required that
deficits persist for at least 24 hours to distinguish
stroke from transient ischemic attack.
• However, transient ischemic attacks usually
resolve within 1 hour.
• In addition, imaging studies can sometimes
demonstrate prior stroke in the absence of
detectable clinical deficits.
 APPROACH TO DIAGNOSIS

• 4. Vascular cause—A vascular cause may be

inferred from the acute onset of symptoms
and often from the patient’s age, the presence
of risk factors for stroke, and the occurrence
of symptoms and signs referable to the
territory of a particular cerebral blood vessel.
• When this is confirmed by imaging studies,
further investigations can be undertaken to
identify a more specific diagnosis.
 ACUTE ONSET

• Strokes begin abruptly.

• Neurologic deficits may be maximal at onset
or may progress over seconds to hours (or
occasionally days).
• A stroke that is actively progressing as a direct
consequence of the underlying vascular
disorder (but not because of associated
cerebral edema) or has done so in recent
minutes is termed stroke in evolution or
progressing stroke.
 ACUTE ONSET

• Focal cerebral deficits that develop slowly

(over weeks to months) are unlikely to be due
to stroke and suggest another process, such as
tumor or inflammatory or degenerative
disease.
 FOCAL INVOLVEMENT

• Stroke produces focal symptoms and signs

that correlate with the area of the brain
supplied by the affected blood vessel.
• In ischemic stroke, occlusion of a blood vessel
interrupts the flow of blood to a specific region
of the brain, interfering with neurologic
functions dependent on that region and
producing a more or less stereotyped pattern
of deficits.
 FOCAL INVOLVEMENT

• Hemorrhage produces a less predictable

pattern of focal involvement because
complications such as increased intracranial
pressure, cerebral edema, compression of
brain tissue and blood vessels, or dispersion
of blood through the subarachnoid space or
cerebral ventricles can impair brain function at
sites remote from the hemorrhage.
 FOCAL INVOLVEMENT

• Global cerebral ischemia (usually from cardiac

arrest) and subarachnoid hemorrhage affect
the brain in more diffuse fashion and produce
global cerebral dysfunction; the term stroke is
not usually applied in these cases.
 FOCAL INVOLVEMENT

• In most cases of stroke, the history and

neurologic examination provide enough
information to localize the lesion to one side
of the brain (eg, to the side opposite a
hemiparesis or hemisensory deficit or to the
left side if aphasia is present) and to the
anterior or posterior cerebral circulation.
 ANTERIOR (CAROTID) CIRCULATION
• The anterior cerebral circulation supplies
most of the cerebral cortex and subcortical
white matter, basal ganglia, and internal
capsule.
• It consists of the internal carotid artery and
its branches: the anterior choroidal, anterior
cerebral, and middle cerebral arteries.
• The middle cerebral artery in turn gives rise
to deep, penetrating lenticulostriate
branches.
 ANTERIOR (CAROTID) CIRCULATION

• Anterior circulation strokes are commonly

associated with symptoms and signs that
indicate hemispheric dysfunction, such as
aphasia, apraxia, or agnosia.
• They also often produce hemiparesis,
hemisensory disturbances, and visual field
defects, but these can occur with posterior
circulation strokes as well.
 POSTERIOR (VERTEBROBASILAR)
CIRCULATION

• The posterior cerebral circulation supplies the

brainstem, cerebellum, thalamus, and portions of the
occipital and temporal lobes.
• It consists of the;
– paired vertebral arteries,
– the basilar artery, and
– their branches:
• the posterior inferior cerebellar,
• anterior inferior cerebellar,
• superior cerebellar, and
• posterior cerebral arteries.
• The posterior cerebral artery also gives off
thalamoperforate and thalamogeniculate branches.
 POSTERIOR (VERTEBROBASILAR)
CIRCULATION

• Posterior circulation strokes produce symptoms and signs of

brainstem or cerebellar dysfunction or both.
 Coma
 Drop attacks (sudden collapse without loss of consciousness),
 Vertigo
 Nausea and vomiting
 Cranial nerve palsies
 Ataxia
 Crossed sensorimotor deficits that affect the face on one side of the
body and the limbs on the other.
• Hemiparesis, hemisensory disturbances, and visual field
deficits also occur, but are not specific to posterior circulation
strokes.
 DURATION OF DEFICITS

• Stroke produces neurologic deficits that

persist.
• When symptoms and signs resolve completely
after briefer periods (usually within 1 hour)
without evidence of cerebral infarction, the
term transient ischemic attack (TIA) is used.
 DURATION OF DEFICITS

• Recurrent TIAs with identical clinical features

(stereotypic TIAs) are usually caused by
thrombosis or embolism arising from the
same site within the cerebral circulation.
• TIAs that differ in character from event to
event suggest recurrent emboli from distant
(eg, cardiac) or multiple sites.
 DURATION OF DEFICITS

• Although TIAs do not themselves produce

lasting neurologic dysfunction, they are
important to recognize because approximately
one-third of patients with TIAs will go on to
have a stroke within 5 years—and because
this risk may be reduced with treatment.
• The underlying pathologic process in stroke
can be either ischemia or hemorrhage, usually
arising from an arterial lesion.
• Ischemia and hemorrhage account for
approximately 90% and 10% of strokes,
respectively.
• It may not be possible to distinguish the two
by history and neurologic examination, but CT
scan or MRI permits definitive diagnosis.
• Among ischemic strokes,
– about 50% are attributed to cardiac embolism,
– 25% to large artery occlusion
– 10% to small artery occlusion
– with the remainder of unknown origin
(cryptogenic).
Cardiac embolism
Leading to ischemic stroke
Large artery occlusion
Leading to ischemic stroke
Small artery occlusion
Leading to ischemic stroke
 ISCHEMIA

• ISCHEMIA
• Interruption of blood flow to the brain deprives
neurons, glia, and vascular cells of substrate
glucose and oxygen.
• Unless blood flow is promptly restored, this
leads to ischemic death of brain tissue
(infarction) within the ischemic core, where
flow is typically less than 20% of normal.
 ISCHEMIA

• Where ischemia is incomplete (20%-40% of

normal blood flow)—as in the ischemic border
zone or penumbra— cell damage is
potentially reversible and cell survival may be
prolonged.
 ISCHEMIA

• However, unless blood flow is restored, by

recanalization of the occluded vessel or
collateral circulation from other vessels,
reversibly damaged cells begin to die as well,
and the infarct expands.
• Death of penumbral tissue is associated with a
worse clinical outcome.
 ISCHEMIA

• Brain edema is another determinant of stroke

outcome.
• Ischemia leads to vasogenic edema as fluid
leaks from the intravascular compartment into
brain parenchyma.
 ISCHEMIA

• Edema is usually maximal approximately 2 to

3 days after stroke and may be sufficiently
severe that it produces a mass effect that
causes herniation (displacement of brain
tissue between intracranial compartments)
and death.
Right hemicraniectomy after brain
edema
 ISCHEMIA

• Two pathogenetic mechanisms can produce

ischemic stroke—thrombosis and embolism.
• However, the distinction is often difficult or
impossible to make on clinical grounds.
 THROMBOSIS

• Thrombosis
• Thrombosis produces stroke by occluding large
cerebral arteries (especially the internal carotid,
middle cerebral, or basilar), small penetrating
arteries (as in lacunar stroke), cerebral veins, or
venous sinuses.
• Symptoms typically evolve over minutes to hours.
• Thrombotic strokes are often preceded by TIAs,
which tend to produce similar symptoms because
they affect the same territory recurrently.
 EMBOLISM

• Embolism
• Embolism produces stroke when cerebral
arteries are occluded by the distal passage of
thrombus from the heart, aortic arch, or large
cerebral arteries.
• Emboli in the anterior cerebral circulation
most often occlude the middle cerebral artery
or its branches, because most hemispheric
blood flow is through this vessel.
 EMBOLISM

• Emboli in the posterior cerebral circulation

usually lodge at the apex of the basilar artery
or in the posterior cerebral arteries.
• Embolic strokes often produce neurologic
deficits that are maximal at onset.
• When TIAs precede embolic strokes, especially
those arising from a cardiac source, symptoms
typically vary between attacks because
different vascular territories are affected.
 HEMORRHAGE

• HEMORRHAGE
• Hemorrhage may interfere with cerebral function
through a variety of mechanisms, including destruction
or compression of brain tissue, compression of
vascular structures, and edema.
• Intracranial hemorrhage is classified by its location as;
– Intracerebral
– Subarachnoid
– Subdural
– Epidural
• all of which—except subdural hemorrhage—are
usually caused by arterial bleeding.
 HEMORRHAGE

• Intracerebral Hemorrhage
• Intracerebral hemorrhage causes symptoms
by destroying or compressing brain tissue.
• Unlike ischemic stroke, intracerebral
hemorrhage tends to cause more severe
headache and depression of consciousness as
well as neurologic deficits that do not
correspond to the distribution of any single
blood vessel.
 HEMORRHAGE

• Subarachnoid Hemorrhage
• Subarachnoid hemorrhage leads to cerebral
dysfunction due to increased intracranial pressure,
resulting hypoperfusion, direct destruction of tissue,
and toxic constituents of subarachnoid blood.
• Subarachnoid hemorrhage may be complicated by
vasospasm (leading to ischemia), rebleeding, extension
of blood into brain tissue (producing an intracerebral
hematoma), or hydrocephalus.
• Subarachnoid hemorrhage typically presents with
headache rather than focal neurologic deficits.
 HEMORRHAGE

• Subdural or Epidural Hemorrhage

• Subdural or epidural hemorrhage produces a
mass lesion that can compress the underlying
brain.
• These hemorrhages are often traumatic in
origin and usually present with headache or
altered consciousness.
 FOCAL CEREBRAL ISCHEMIA

• PATHOPHYSIOLOGY
• The pathophysiology of focal cerebral ischemia
is complex, as it involves a process that evolves
over time, affects the brain nonuniformly, and
targets multiple cell types.
 CLINICAL-ANATOMIC CORRELATION

• Infarction in the distribution of different

cerebral arteries often produces distinctive
clinical syndromes, which can facilitate
anatomic and etiologic diagnosis and help
guide treatment.
 ANTERIOR CEREBRAL ARTERY

• ANTERIOR CEREBRAL ARTERY

• Anatomy
• The anterior cerebral artery supplies the
parasagittal cerebral, which includes portions
of motor and sensory cortex related to the
contralateral leg, the so-called bladder
inhibitory or micturition center, and the
anterior corpus callosum.
 ANTERIOR CEREBRAL ARTERY

• Clinical Syndrome
• Anterior cerebral artery strokes produce
contralateral paralysis and sensory loss
exclusively or primarily affecting the leg.
• There may also be abulia (apathy),
disconnection syndromes such as the alien
hand (involuntary performance of complex
motor activity), transcortical expressive
aphasia, and urinary incontinence.
 MIDDLE CEREBRAL ARTERY

• MIDDLE CEREBRAL ARTERY

• Anatomy
• The middle cerebral artery supplies most of
the remainder of the cerebral hemisphere and
deep subcortical structures
 MIDDLE CEREBRAL ARTERY

• Cortical branches include the superior

division, which supplies motor and sensory
representation of the face, hand, and arm,
and the expressive language (Broca) area of
the dominant hemisphere.
• The inferior division supplies the visual
radiations, visual cortex related to macular
vision, and the receptive language (Wernicke)
area of the dominant hemisphere.
MCA superior
division enfarct

MCA inferior
division enfarct
 MIDDLE CEREBRAL ARTERY

• Lenticulostriate branches of the most

proximal portion (stem) of the middle cerebral
artery supply;
• the basal ganglia and
• motor fibers to the face, hand, arm, and leg
• as they descend in the genu and the posterior
limb of the internal capsule.
 MIDDLE CEREBRAL ARTERY

• Clinical Syndrome
• Depending on the site of involvement, several
clinical syndromes can occur.
• 1. Superior division stroke results in contralateral
hemiparesis that affects the face, hand, and arm
but spares the leg, and contralateral hemisensory
deficit in the same distribution, but no
homonymous hemianopia.
• If the dominant hemisphere is involved, there is
Broca (expressive) aphasia, which is characterized
by impaired language expression with intact
comprehension.
 MIDDLE CEREBRAL ARTERY

• 2. Inferior division stroke results in contralateral

homonymous hemianopia that may be denser
inferiorly, impaired cortical sensory functions (eg,
graphesthesia and stereognosis) on the
contralateral side of the body, and disorders of
spatial thought (eg, anosognosia [unawareness of
deficit], neglect of the contralateral limbs and
contralateral side of external space, dressing
apraxia, and constructional apraxia).
 MIDDLE CEREBRAL ARTERY

• If the dominant hemisphere is involved,

Wernicke (receptive) aphasia occurs and is
manifested by impaired comprehension and
fluent but often nonsensical speech.
• With involvement of the nondominant
hemisphere, an acute confusional state may
occur.
 MIDDLE CEREBRAL ARTERY

• 3. Occlusion at the bifurcation or trifurcation

of the middle cerebral artery combines the
features of superior and inferior division
stroke, including contralateral hemiparesis and
hemisensory deficit involving the face and arm
more than leg, homonymous hemianopia,
and—if the dominant hemisphere is
affected—global (combined expressive and
receptive) aphasia.
 MIDDLE CEREBRAL ARTERY

• 4. Occlusion of the stem of the middle

cerebral artery occurs proximal to the origin
of the lenticulostriate branches, resulting in a
clinical syndrome similar to that seen after
occlusion at the trifurcation.
• In addition, however, involvement of the
internal capsule causes paralysis of the
contralateral leg, so hemiplegia and sensory
loss affect face, hand, arm, and leg.
 INTERNAL CAROTID ARTERY

• INTERNAL CAROTID ARTERY

• Anatomy
• The internal carotid artery arises at the
bifurcation of the common carotid artery in
the neck.
• In addition to the anterior and middle cerebral
arteries, it also gives rise to the ophthalmic
artery, which supplies the retina.
 INTERNAL CAROTID ARTERY

• Clinical Syndrome
• Internal carotid artery occlusion may be
asymptomatic, or cause strokes of highly variable
severity, depending on the adequacy of collateral
circulation.
• Symptomatic occlusion results in a syndrome
similar to that of middle cerebral artery stroke
(contralateral hemiplegia, hemisensory deficit,
and homonymous hemianopia, together with
aphasia if the dominant hemisphere is involved).
• Monocular blindness is also common.
 POSTERIOR CEREBRAL ARTERY

• POSTERIOR CEREBRAL ARTERY

• Anatomy
• The paired posterior cerebral arteries arise from
the tip of the basilar artery in most cases and
supply the occipital cerebral cortex, medial
temporal lobes, posterior corpus callosum,
thalamus, and rostral midbrain.
• Emboli in the basilar artery tend to lodge at its
apex and occlude one or both posterior cerebral
arteries; subsequent fragmentation can produce
asymmetric or patchy posterior cerebral artery
infarction.
 POSTERIOR CEREBRAL ARTERY

• Clinical Syndrome
• Posterior cerebral artery occlusion produces
homonymous hemianopia affecting the
contralateral visual field, except that macular
vision may be spared.
• In contrast to visual field defects from
infarction in the middle cerebral artery
territory, those caused by posterior cerebral
artery occlusion may be denser superiorly.
 POSTERIOR CEREBRAL ARTERY

• With occlusion near the origin of the posterior

cerebral artery at the level of the midbrain,
ocular abnormalities may occur, including
vertical gaze palsy, oculomotor (III) nerve
palsy, internuclear ophthalmoplegia, and
vertical skew deviation of the eyes.
 POSTERIOR CEREBRAL ARTERY

• Involvement of the occipital lobe of the dominant

hemisphere may cause anomic aphasia (difficulty
in naming objects), alexia without agraphia
(inability to read, with no impairment of writing),
or visual agnosia.
• The last is failure to identify objects presented in
the left side of the visual field, caused by a lesion
of the corpus callosum that disconnects the right
visual cortex from language areas of the left
hemisphere.
 POSTERIOR CEREBRAL ARTERY

• Bilateral posterior cerebral artery infarction

may result in cortical blindness, memory
impairment (from temporal lobe
involvement), or inability to recognize familiar
faces (prosopagnosia), as well as a variety of
exotic visual and behavioral syndromes.
 BASILAR ARTERY

• BASILAR ARTERY
• Anatomy
• The basilar artery arises from the junction of the paired
vertebral arteries and courses over the ventral surface of
the brainstem to terminate at the level of the midbrain,
where it bifurcates to form the posterior cerebral arteries.
• Branches of the basilar artery supply;
– the occipital lobe
– medial temporal lobes
– medial thalamus
– posterior limb of the internal capsule
– brainstem
– cerebellum
• Clinical Syndromes
• 1. Thrombosis—Thrombotic occlusion of the
basilar artery or both vertebral arteries is
often incompatible with survival.
• It causes bilateral symptoms and signs of
brainstem and cerebellar dysfunction from
involvement of multiple branch arteries.
• 1. Thrombosis
• Basilar thrombosis usually affects the proximal
basilar artery, which supplies the pons.
• Involvement of the dorsal pons (tegmentum)
produces unilateral or bilateral abducens (VI)
nerve palsy; horizontal eye movements are
impaired, but vertical nystagmus and ocular
bobbing may be present.
• The pupils are constricted due to involvement of
descending sympathetic pupillodilator fibers, but
may be reactive.
• 1. Thrombosis
• Hemiplegia or quadriplegia is usually present,
and coma is common.
• In some patients, the ventral pons (basis
pontis) is infarcted and the tegmentum is
spared.
• Such patients remain conscious but
quadriplegic (locked-in syndrome).
• Locked-in patients may be able to open or
move their eyes vertically on command.
• 2. Embolism—Emboli in the basilar artery usually
lodge at its apex.
• Interruption of blood flow to the ascending
reticular formation in the midbrain and thalamus
produces immediate loss or impairment of
consciousness.
• Unilateral or bilateral oculomotor (III) nerve
palsies are characteristic.
• Hemiplegia or quadriplegia with decerebrate or
decorticate posturing results from involvement of
the cerebral peduncles in the midbrain.
• LACUNAR INFARCTION
• Anatomy
• Small vessel occlusion affecting penetrating arteries
deep in the brain may cause infarcts in;
– the putamen
– the thalamus
– caudate nucleus
– pons
– posterior limb of the internal capsule
– other sites
• These are referred to as lacunar infarcts or lacunes.
• Clinical Syndromes
• Many lacunar infarcts are not recognized
clinically and are detected only as incidental
findings on imaging studies or at autopsy.
• In other cases, however, they produce
distinctive clinical syndromes.
• Lacunar strokes develop over hours to days.
• Headache is absent or minor, and the level of
consciousness is unchanged.
• Hypertension, diabetes, and other
cardiovascular risk factors may or may not be
present.
• The prognosis for recovery from a lacunar
stroke is good, but recurrent stroke is
common.
• Although a variety of deficits can be produced,
there are four classic and distinctive lacunar
syndromes.
• 1. Pure motor hemiparesis—
• This consists of hemiparesis affecting the face,
arm, and leg to a roughly equal extent, without
associated disturbance of sensation, vision, or
language.
• Lacunes that produce this syndrome are usually
located in the contralateral internal capsule or
pons.
• 2. Pure sensory stroke—
• This is characterized by hemisensory loss,
which may be associated with paresthesia,
and results from lacunar infarction in the
contralateral thalamus.
• 3. Ataxic hemiparesis—
• In this syndrome, sometimes called ipsilateral
ataxia and crural (leg) paresis, pure motor
hemiparesis is combined with ataxia of the
hemiparetic side and usually affects the leg
predominantly.
• Symptoms result from a lesion in the
contralateral pons, internal capsule, or
subcortical white matter.
• 4. Dysarthria-clumsy hand syndrome—
• This consists of dysarthria, facial weakness,
dysphagia, and mild weakness and
clumsiness of the hand on the side of facial
involvement.
• Lacunes causing this syndrome are located in
the contralateral pons or internal capsule.
• ETIOLOGY
• Focal cerebral ischemia can result from
underlying disorders that primarily affect the
blood, blood vessels, or heart.
• VASCULAR DISORDERS
• Atherosclerosis
• Atherosclerosis of the large extracranial
arteries in the neck and at the base of the
brain and of smaller intracranial arteries is a
common cause of focal cerebral ischemia.
• The pathogenesis of atherosclerosis is
incompletely understood, but endothelial cell
dysfunction is thought to be an early step.
• This tends to occur at sites of low or disturbed
blood flow, such as arterial curvatures and
branch points.
• Major risk factors for atherosclerosis leading to
stroke include;
– systolic or diastolic hypertension
– elevated serum LDL cholesterol
– diabetes mellitus
• Current recommendations are;
• to reduce blood pressure to <140 mm Hg systolic
and <90 mm Hg diastolic (<130 systolic and <80
diastolic if other risk factors are present),
• hold LDL cholesterol below 160 mg/dL (lower
with other risk factors)
• maintain pre- and postprandial capillary blood
glucose concentrations at 90-126 and <180
mg/dL, respectively.
• These goals may be achieved by lifestyle
change, dietary modification, or
pharmacotherapy (eg, antihypertensives,
statins, oral hypoglycemic drugs, or insulin).
• CLINICAL FINDINGS
• HISTORY
• Predisposing Factors
• Risk factors such as TIAs, hypertension,
diabetes, dyslipidemia, ischemic or valvular
heart disease, cardiac arrhythmia, cigarette
smoking, and oral contraceptive use should be
sought.
• Hematologic and other systemic disorders can
also increase the risk of stroke.
• Antihypertensive drugs can precipitate
cerebrovascular symptoms if the blood
pressure is lowered excessively in patients
with nearly total cerebrovascular occlusion
and poor collateral circulation.
• Onset & Course
• The history should establish the time of onset of
symptoms.
• whether similar symptoms have occurred before;
and
• whether the clinical picture is that of TIA, stroke
in evolution, or completed stroke.
• Associated Symptoms
• 1. Headache is present at onset in about 25%
of patients with ischemic stroke and is
especially common in intracranial arterial
dissection and venous or sinus thrombosis.
• 2. Seizures can accompany the onset of stroke
or follow stroke by weeks to years, but do not
definitively distinguish embolic from
thrombotic stroke.
• PHYSICAL EXAMINATION
• General Physical Examination
• The general physical examination should focus on
searching for an underlying systemic (especially
treatable) cause of cerebrovascular disease.
• 1. The blood pressure should be measured to detect
hypertension—a major risk factor for stroke.
• 2. Comparison of blood pressure and pulse on the
two sides can reveal differences related to
atherosclerotic disease of the aortic arch.
• 3. Ophthalmoscopic examination of the retina can
provide evidence of embolization in the anterior
circulation, in the form of visible embolic material in
retinal blood vessels.
• 4. Neck examination may reveal the absence of
carotid pulses or the presence of carotid bruits.
• However, reduced carotid artery pulsation in the
neck is a poor indicator of internal carotid artery
disease, significant carotid stenosis can occur
without an audible bruit, and a loud bruit can
occur without stenosis.
• 5. Cardiac examination can detect arrhythmias, or
murmurs related to valvular disease, which may
predispose to cardioembolic stroke.
• Neurologic Examination
• Patients with cerebrovascular disorders may
or may not have abnormal neurologic findings.
• A normal examination is expected, for
example, after a TIA has resolved.
• Where deficits are found, the goal is to define
the anatomic site of the lesion, which may
suggest the cause or optimal management of
stroke.
• 1. Cognitive deficits such as aphasia,
unilateral neglect or constructional apraxia
suggest a cortical lesion in the anterior
circulation and exclude vertebrobasilar or
lacunar stroke.
• Coma implies brainstem or bihemispheric
involvement.
• 2. Visual field abnormalities also exclude lacunar
infarction, but hemianopia can occur with
occlusion of either the middle or posterior
cerebral artery, which supply the optic radiation
and visual cortex, respectively.
• Isolated hemianopia suggests posterior cerebral
artery stroke, because middle cerebral artery
stroke should produce additional (motor and
somatosensory) deficits.
• 3. Ocular palsy, nystagmus, or internuclear
ophthalmoplegia assigns the underlying
lesion to the brainstem and thus the posterior
cerebral circulation.
• 4. Hemiparesis can be due to lesions in
cerebral cortical regions supplied by the
anterior circulation, descending motor
pathways in the brainstem supplied by the
vertebrobasilar system, or lacunes at
subcortical or brainstem sites.
• Hemiparesis affecting the face, hand, and arm
more than the leg is characteristic of middle
cerebral artery lesions.
• Crossed hemiparesis, which involves the face
on one side and the rest of the body on the
other, assigns the lesion to the brainstem
between the facial (VII) nerve nucleus in the
pons and the decussation of the pyramids in
the medulla.
• 5. Cortical sensory deficits such as
astereognosis or agraphesthesia, with
preserved primary sensory modalities, imply a
cortical deficit within the middle cerebral
artery territory.
• Hemisensory deficits without associated
motor involvement are usually lacunar.
• Crossed sensory deficits result from lesions in
the medulla, as seen in the lateral medullary
syndrome.
• 6. Hemiataxia usually points to a lesion in the
ipsilateral brainstem or cerebellum but can
also be produced by lacunar stroke in the
internal capsule.
• INVESTIGATIVE STUDIES
• BLOOD TESTS
• Serum Glucose
• Hypoglycemia and hyperglycemia can both present
with focal neurologic signs and masquerade as
stroke.
• Hypoglycemia requires immediate administration
of glucose to avoid permanent brain injury.
• Hyperglycemia also requires prompt specific
treatment.
• Complete Blood Count
• This can identify possible causes of stroke (eg,
thrombocytosis, polycythemia, sickle cell
disease) or suggest concomitant infection,
which may complicate its course.
• A platelet count less than 100,000/μL
contraindicates thrombolytic therapy for
stroke.
• Coagulation Studies
• Coagulation defects due to anticoagulant drugs
or liver dysfunction may affect eligibility for
thrombolytic therapy and other aspects of
management.
• Inflammatory Markers
• An increased erythrocyte sedimentation rate
(ESR) is seen in giant cell arteritis and other
systemic vasculitides.
• Circulating Troponin Level
• Myocardial infarction, which requires specific
management, should be excluded by
measuring troponin as a marker of myocardial
ischemia, as well as by electrocardiogram.
• ELECTROCARDIOGRAM (ECG)
• An ECG should be obtained routinely to detect
unrecognized myocardial infarction or cardiac
arrhythmias, such as atrial fibrillation, which
predispose to stroke.
• LUMBAR PUNCTURE
• Lumbar puncture should be performed only in
selected cases, to exclude subarachnoid
hemorrhage (manifested by xanthochromia
and red blood cells).
• BRAIN IMAGING
• A CT scan or MRI should be obtained routinely
(and always prior to thrombolytic therapy), to
distinguish between infarction and
hemorrhage as the cause of stroke, to exclude
other lesions (eg, tumor, abscess) that can
mimic stroke, and to localize the lesion.
• Noncontrast CT is usually preferred for initial
diagnosis because it is widely available and rapid
and can readily make the critical distinction
between ischemia and hemorrhage.
• However, its sensitivity within the first 6 hours is
limited.
• MRI may be superior to CT scan for
demonstrating early ischemic infarcts, showing
ischemic strokes in the brainstem or cerebellum,
and detecting thrombotic occlusion of venous
sinuses.
• Diffusion-weighted MRI (DWI) and perfusion
weighted MRI (PWI) are additional imaging
techniques that may be useful for early
detection and prognostication in stroke.
• DWI is superior to CT for detecting stroke
during the first 12 hours after onset and may
help predict final infarct volume in anterior
circulation stroke, although diffusion defects
are sometimes seen with TIAs, and small
strokes or brainstem strokes may escape
detection.
• The difference between DWI and PWI
abnormalities (diffusion-perfusion mismatch)
may represent tissue that is at risk of
infarction but potentially salvageable by
thrombolysis, which equates roughly to the
ischemic penumbra.
• VESSEL IMAGING
• Imaging techniques can identify underlying
causes of cerebrovascular disease (eg, carotid
stenosis, vasculitis, fibromuscular dysplasia,
arterial dissection, aneurysm, arteriovenous
malformation), including operable extracranial
carotid lesions.
• Doppler ultrasonography can detect operable
stenosis of the extracranial carotid artery and is
noninvasive.
• However, it may not distinguish stenosis from
occlusion and does not visualize the
surrounding vascular anatomy, so it is used
primarily for screening.
• Digital subtraction angiography is more sensitive
and specific, but carries a small (<1%) risk of
serious complications, including stroke.
• Magnetic resonance angiography (MRA) is a
noninvasive substitute for digital subtraction
angiography and can detect extracranial carotid
disease with high sensitivity and specificity.
• CT angiography is an alternative, but involves
radiation exposure and may be obscured by
artifact from calcium in atherosclerotic plaques.
• ECHOCARDIOGRAPHY
• Echocardiography may be useful for
demonstrating cardiac lesions responsible for
embolic stroke (eg, mural thrombus, valvular
disease, or atrial myxoma).
• DIFFERENTIAL DIAGNOSIS
• Disorders sometimes mistaken for ischemic
stroke include intracerebral hemorrhage,
subdural or epidural hematoma, subarachnoid
hemorrhage, brain tumor and brain abscess,
which can be excluded by CT scan or MRI.
• Metabolic disturbances such as hypoglycemia
and hyperosmolar nonketotic hyperglycemia may
present in stroke-like fashion, but the serum
glucose level is diagnostic.
 PRIMARY PREVENTION

• Lifestyle
• Moderate to vigorous aerobic activity for 30
to 40 min per day, 3 to 4 times per week, is
recommended.
• A diet low in sodium and saturated fats and
rich in fruits, vegetables, low-fat dairy
products, and nuts may also reduce stroke
risk, as may weight reduction in overweight or
obese alcohol use.
 PRIMARY PREVENTION

• Statins
• Treatment with a statin is recommended for patients,
with or without dyslipidemia, who are at increased
(>10%) 10-year risk for cardiovascular events, including
stroke.
• Risk is assessed based on sex, age, race, total and HDL
cholesterol, systolic blood pressure, antihypertensive
therapy, diabetes, and smoking history.
• This approach reflects the finding that statins have
vasoprotective (eg, anti-inflammatory) actions besides
their lipid-lowering effects.
 PRIMARY PREVENTION

• Blood Pressure Control

• Blood pressure should be reduced by lifestyle
modification, antihypertensive drugs, or both for
patients with hypertension (>140 mm Hg systolic or
>90 mm Hg diastolic pressure).
• Glycemic Control
• Diabetes increases the risk of stroke and should be
treated, although the relationship between intensity of
glycemic control and stroke incidence is unclear.
• In addition to whatever effect glycemic control may
have, stroke risk in diabetics can be reduced by statins
and antihypertensive treatment.
 PRIMARY PREVENTION

• Antiplatelet Drugs
• Low-dose aspirin (81-100 mg/d) may reduce
the risk of stroke in patients with increased
(>10%) 10-year risk for such events .
• Anticoagulation
• Anticoagulation is indicated for patients with
certain cardiac disorders that predispose to
stroke, assuming an acceptably low likelihood
of hemorrhagic complications.
 PRIMARY PREVENTION

• Asymptomatic Carotid Artery Stenosis

• Asymptomatic 70% to 99% stenosis of the extracranial
internal carotid artery or carotid bulb (but not total
carotid occlusion) is also associated with an increased
risk of stroke, and patients with asymptomatic stenosis
should be treated with low-dose aspirin and statins.
• In some cases with >70% stenosis, carotid
endarterectomy or carotid artery stenting (discussed
later) may be employed, assuming that a surgical
complication rate of 3% or less can be anticipated.