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Stroke In The Young Adult

What Is A Stroke ?

A stroke occurs when blood flow to


the brain is interrupted by a blocked
or a ruptured blood vessel.
A brain attack.

Stroke

Acute stroke is typically


characterized by the sudden onset of
a focal neurologic deficit, though
some patients have a stepwise or
gradual progression of symptoms.

Stroke

Common deficits include:


Dysphasia (difficulty swallowing)
Dysarthria (difficulty speaking)
Hemianopia (difficulty with sight)
Weakness

Stroke Common Deficits

Ataxia
Sensory loss
Neglect
Consciousness is generally normal
but maybe impaired

Stroke Warning Signs

Sudden weakness or numbness of the


face, arm or leg, especially on one side
of the body
Sudden confusion, trouble speaking or
understanding
Sudden trouble seeing in one or both
eyes

Stroke Warning Signs

Sudden trouble walking, dizziness,


loss of balance or coordination
Sudden, severe headaches with no
known cause (for hemorrhagic
stroke)

Stroke Warning Signs

Acute loss of focal cerebral function


Abrupt onset
Symptoms occur in all affected areas at
the same time
Symptoms resolve gradually
Symptoms are negative

Nature of Symptoms

Positive symptoms indicate active discharge


from central nervous system neurons. Typical
positive symptoms can be visual (e.g., bright
lines, shapes, objects), auditory (e.g.,
tinnitus, noises, music), somatosensory (e.g.,
burning, pain, paresthesias), or motor (e.g.,
jerking or repetitive rhythmic movements).
Negative symptoms indicate an absence or
loss of function, such as loss of vision,
hearing, feeling, or ability to move a part of
the body.

Annual Incidence of Ischemic


Stroke

In young adults (1545 years) has been


estimated at approximately 211 per
100,000 in Caucasians, 22.8 per 100,000
in African Americans
10/100,000 in a Mayo Clinic study of
women ages 15 to 29
About 212% of cerebral infarcts occur in
young adult patients, with a higher
frequency between 31 and 45 years

Annual Incidence of Ischemic


Stroke

Stroke ranks second after ischemic


heart disease as a cause of lost
disability-adjusted life-years in highincome countries

Mortality of Strokes

Mortality in the first month after stroke


has been reported to range from 2.5% in
patients with lacunar infarcts to 78% in
patients with space-occupying hemispheric
infarction.
Lacunar stroke or lacunar infarct
(LACI) is a type of stroke that results
from occlusion of one of the penetrating
arteries that provides blood to the brain's
deep structures.

Stroke

Stroke in young adults is surprisingly


common.
The differential diagnosis for
potential etiologies is broader than
that for older adults.

Stroke

In children and young adults;


Congenital and acquired heart
problems,
Hematologic conditions,
Vasculopathies,
Metabolic disorders,
Drug ingestion
are more common.

Causes of Stroke

The largest series studies of young


adults with ischemic stroke cite
undetermined as the most frequent
etiology (up to 35% of patients)
Ischemic stroke is much more
common than hemorrhagic

Causes of Stroke

Up to 45% of strokes in young adults


are due to spontaneous intracerebral
hemorrhage.
Vascular malformations, aneurysms,
hypertension, and illicit drug use are
the main causes.

Causes of Ischemic Stroke in Young


Adults Eur Neurol 2007;57:212218

Cardiovascular Risk Factors in


272 Young Patients % (n)

Major cardiovascular risk factors 35 (96)


Arterial hypertension 22 (59)
Diabetes mellitus 8 (21)
Hypercholesterolemia 17 (46)
Atherosclerosis 5 (14)
Causes of Ischemic Stroke in Young Adults
Eur Neurol 2007;57:212218

Cardiovascular Risk Factors in


272 Young Patients % (n)

Minor cardiovascular risk factors 63


(172)
Cigarette smoking 49 (133)
Oral contraceptives 18 (17)
High alcohol intake 31 (84)
Causes of Ischemic Stroke in Young
Adults Eur Neurol 2007;57:212218

Prevention of Stroke

Control high blood pressure


Prevent heart disease
Stop cigarette smoking
Recognize signs of TIA
Reduce blood cholesterol levels

Stroke Risk Factors That Can Be


Treated

Hypertension/High Blood Pressure

Heart Disease

Cigarette Smoking

Transient Ischemic Attacks

Stroke Risk Factors That Can Be


Treated

Diabetes

Elevated Blood Cholesterol/Lipids

Asymptomatic Carotid Bruits

Stroke Risk Factors


That Cannot Be Treated

Age
Gender
Race
Prior stroke
Family history

Stroke Risk Factors Less WellDocumented

Geographical Location

Socioeconomic Factors

Excessive Alcohol Intake

Certain Kinds of Drug Abuse

What Are the Types of Stroke ?


Ischemic Stroke (Blockage)
Caused by a blockage in blood
vessels in brain
Hemorrhagic Stroke (Bleeding)
Caused by ruptured or leaking blood
vessels in brain

Stroke Background
Inadequate blood flow

Ischemic stroke
Focal thrombotic or embolic occlusion of
major artery
Global inadequate cerebral perfusion

Hemorrhage
Parenchymal into brain tissue
Subarachnoid surrounding subarachnoid
space

Causes of Stroke

Some of the most common causes of


ischemia in the young
Cardioembolism (2035%),
Dissection of extracranial arteries (6
25%),
Migraine with aura (120%)
Drugs (10%)
Hypercoagulable states (510%)
Premature atherosclerosis (20-25%)

Ischemic Stroke

In patients younger than 55 years,


only about 10% of strokes are
caused by large-vessel
atherosclerotic disease.

What Are the Causes of Ischemic


Stroke?
Large vessel disease

Premature atherosclerosis
Dissection (spontaneous or traumatic)
Inherited metabolic diseases (homocystinuria, Fabrys, pseudoxanthoma
elasticum, MELAS syndrome)
Fibromuscular dysplasia
Infection (bacterial, fungal, tuberculosis, syphilis, Lyme)
Vasculitis (collagen vascular diseases systemic lupus erythematosus,
rheumatoid arthritis, Sjgrens syndrome, polyarteritis nodosa; Takayasus
disease, Wegeners syndrome, cryoglobulinemia, sarcoidosis, inflammatory
bowel disease, isolated central nervous system angiitis)
Moyamoya disease: (Japanese, "puff of cigar smoke") is an inherited
disease in which certain arteries in the brain are constricted
Radiation
Toxic (illicit drugs cocaine, heroin, phencyclidine; therapeutic drugs Lasparaginase, cytosine arabinoside, ephedra, phenylephrine)

What Are the Causes of Ischemic


Stroke?

Cardiac disease (including


congenital, rheumatic valve disease,
mitral valve prolapse, patent
foramen ovale, endocarditis, atrial
myxoma, arrhythmias, cardiac
surgery)

What Are the Causes of Ischemic


Stroke?

Small vessel disease


Vasculopathy (infectious,
noninfectious, microangiopathy)
Independent predictors of
arteriopathy are sickle cell disease
and recent upper respiratory
infection.

What Are the Causes of Ischemic


Stroke?

Hematologic disease
Sickle-cell disease
Leukemia
Hypercoagulable states (antiphospholipid antibody
syndrome, deficiency of antithrombin III or protein S or C,
resistance to activated protein C, increased factor VIII)
Disseminated intravascular coagulation
Thrombocytosis
Polycythemia vera
Thrombotic thrombocytopenic purpura
Venous occlusion (dehydration, parameningeal infection,
meningitis, neoplasm, polycythemia, leukemia,
inflammatory bowel disease)

Hematologic Disorders

Many hematologic disorders are


associated with ischemic stroke.
The disorders most likely to cause
ischemic stroke in patients younger
than 45 years are:
Antiphospholipid antibody syndrome
Sickle cell anemia
Heparin induced thrombocytopenia

APS

Antiphospholipid syndrome (APS or APLS) or


antiphospholipid antibody syndrome is a
disorder of coagulation that causes blood clots
(thrombosis) in both arteries and veins as well as
pregnancy-related complications such as
miscarriage, stillbirth, preterm delivery, or severe
preeclampsia. The syndrome occurs due to the
autoimmune production of antibodies against
phospholipid (aPL), a cell membrane substance.
In particular, the disease is characterized by
antibodies against cardiolipin (anti-cardiolipin
antibodies) and 2 glycoprotein.

Hematologic disorders

Most of the common hereditary


hypercoagulable disorders, such as
factor V Leiden/activated protein C
resistance, the prothrombin gene
mutation (G20210A), antithrombin
III deficiency, protein C deficiency,
and protein S deficiency, typically
cause venous thrombosis much more
often than they cause arterial
thrombosis.

What Are the Causes of Ischemic


Stroke?
Migraine: especially with aura

Embolism:
Cardiogenic (atrial fibrillation,
mural thrombus, myxoma,
valvular vegetations)
Artery-to-artery
Fat
Air
Paradoxical (emboli of
venous origin passing through
a patent foramen ovale)

Cardiogenic Embolism

Major risk factors:

Anticoagulation

Indicated
Atrial fibrillation
Mitral stenosis
Prosthetic cardiac valve
Recent MI
Thrombus in LV or LA appendage
Atrial myxoma
Infective endocarditis (No anticoagulation)
Dilated cardiomyopathy

Cardiogenic Embolism

Minor risk factors:

Best treatment unclear


Pathologic Mitral valve prolapse (2% of
population)
Mitral annular calcification
Patent foramen ovale (25% 0f population)
Atrial septal aneurysm
Calcific aortic stenosis
LV regional wall motion abnormality
Aortic arch atheromatous plaques
Spontaneous echocardiographic contrast

Cardiogenic Embolism

One-fifth to one-third of strokes in


the young may be caused by
cardioembolic phenomena.

Cardiogenic Embolism

Paradoxical embolization
from the right heart to the left is
believed to occur via a patent
foramen ovale or atrial septal
defect (which can be found on
autopsy in up to one fourth of all
people.

Atherosclerosis of the
aorta or carotid arteries
can be a source of both
atheroemboli and
thromboemboli

Cardiogenic Embolism

Left atrial thrombi


account for nearly half
of cardiac
thromboemboli. The
most common cause is
atrial fibrillation; other
causes are dilated
cardiomyoapthy,
mitral valve stenosis,
and some
hypercoagulable
states.

Left
atrium

Right
atrium

Left atrium

Valsalva

Figure 1. Transesophageal Echocardiograms of a


Patent Foramen Ovale.
In Panel A, a transesophageal echocardiogram in the
Right
atrium the
longitudinal plane shows a separation
between
primum septum (arrowhead) and the secundum septum
a finding consistent with the presence of patent
foramen ovale.
Panel B shows a transesophageal echocardiogram, also in
the longitudinal plane, obtained during the injection of
agitated-saline contrast material through an antecubital
vein with use of the Valsalva maneuver. There is
complete opacification of the right atrium, and passage of
a cloud of bubbles between the primum and secundum
septa into the left atrium is visible.

RA

LA

Figure 2. Transesophageal echocardiogram showing a thrombus (arrows)


passing from right atrium (RA) to left atrium (LA) through a patent foramen
ovale.

Right
atrium

Left
atrium

Left
atrium
Left
ventricle

Right
atrium

Right
ventricle

Figure 2. Transesophageal Echocardiograms of an Atrial Septal


Aneurysm.
In Panel A, a transesophageal echocardiogram (in the horizontal plane)
shows an atrial septal aneurysm protruding into the right atrium (arrow).
Atrial septal aneurysm is defined as either sustained bowing of a 15-mm
segment of interatrial septal membrane in the fossa ovalis of at least 11 mm
(or at least 15 mm by a more conservative definition) beyond the plane of
the interatrial septum or as phasic excursion to either side totaling the same
distance.
Panel B shows a transesophageal echocardiogram showing the same atrial
septal aneurysm (arrow) viewed in the longitudinal plane.

PFO

Figure 3. Percutaneous Closure of a Patent Foramen


Ovale.
With use of a femoral approach, a transvenous sheath is
advanced across the foramen into the left atrium, where a
folded disk is expanded and pulled back, apposing the
primum and secundum septa closed. This step is followed
by deployment of a right-sided disk, at which time the twodisk device is released. Clopidogrel and aspirin are
recommended for a period of three months to prevent
thrombus formation on the device, with aspirin therapy
continued for an additional three months, when
endothelialization is complete. Antibiotic prophylaxis for six
months is recommended. Complete late closure of the
foramen has been reported in 80 to 95 percent of patients.

Cocaine Abuse

Another important cause of ischemic stroke is the


use of sympathomimetic drugs such as cocaine
amphetamines, ephedra, or phenylephrine. The
strongest association is with cocaine, which has
been seen in case series to cause cerebral
vasoconstriction in a dose-dependent manner.
Vasoconstriction is also related to a longer
duration of cocaine use. Several case-control
studies have found that the risk of stroke is 4.5 to
6.5 times higher in drug abusers than in controls,
and that use of catecholamines or cocaine alone
was associated with a significantly increased risk
of stroke.

What Are the Causes of


Hemorrhagic Stroke?
Occurs when a weakened blood
vessel ruptures
Aneurysms: Ballooning of a
weakened region of a blood vessel
Arteriovenous Malformations (AVMs):
Cluster of abnormal blood vessels

Arteriovenous Malformations

Cerebral AVMs are most commonly


discovered in young adults aged 20-40
years.
These lesions are usually detected in
patients as the result of a seizure or
hemorrhage.
AVMs hemorrhage at a rate of 4% per
year.
Approximately half of these hemorrhages
will carry significant morbidity or mortality.

HEMORRHAGIC

Arteriovenous malformation
Neoplasm (primary central nervous
system, metastatic, leukemia)
Hematologic (sickle-cell disease,
neoplasm, thrombocytopenia)
Moyamoya disease
Drug use (warfarin, amphetamines,
cocaine, phenypropanolamine)
Iatrogenic (peri-procedural)

Moyamoya

Moyamoya syndrome is characterized by progressive


stenosis of the internal carotid arteries and formation of
collateral vessels that give a "puff of smoke" appearance on
angiography.
Moyamoya disease occurs mainly in Japanese and other
Asian populations and may have a genetic basis.
Secondary moyamoya syndrome is seen in association with
neurofibromatosis, Down syndrome, Williams syndrome,
sickle cell disease, and as a sequela of cranial irradiation.
Intracranial hemorrhage is common in young adults.
Dissection Arterial dissection is the most common
vascular abnormality in some young adult series

Intracerebral Hemorrhage

Diffuse subarachnoid hemorrhage


Focal intraparenchymal
Accounts for 20% of all strokes
Acute rise in intracranial pressure
from arterial rupture frequently
results in loss of consciousness at
outset
Some patients die from herniation

Causes of Spontaneous
Intracerebral Hemorrhage
(ICH)

Intraparenchymal hemorrhage
Trauma
Hypertension
Amyloid angiopathy
Arteriovenous malformation
Bleeding diathesis (anticoagulants,
thrombolytics)
Drugs (amphetamines, cocaine)

Causes of Spontaneous
Intracerebral Hemorrhage
Cervical arterial
(ICH)
dissection causes up

to 20% of strokes in patients


younger than 45 years.
Dissections usually involve the
extracranial portion of the vessel,
and involve the internal carotid
arteries at least three times as often
as the vertebral arteries.

Causes of Spontaneous
Intracerebral Hemorrhage
In many cases the dissection is preceded
(ICH)

by mild neck trauma, which may be as


minor as a vigorous cough or turning of
the head.
Typical features of dissection include: Neck
pain, headache, and Horner syndrome,
followed minutes to hours later by
symptoms of ocular or cerebral ischemia,
usually a transient ischemic attack rather
than a stroke.

Causes of Spontaneous
Intracerebral Hemorrhage
Inherited disorders
that are
(ICH)

associated with increased risk of


cervical arterial dissection include:
Ehlers-Danlos syndrome type IV
Marfan syndrome
Autosomal dominant polycystic
kidney disease
Osteogenesis imperfecta type I
Fibromuscular dysplasia

Diagnosis, Management,
and Prognosis of ICH

CT diagnostic test of choice


Hyperintense area with mass effect and
later hypointense surrounding edema

MRI less sensitive in early stages

Diagnosis, Management,
and Prognosis of ICH

Management depends on size


and location
In acute phase, mass effect far greater
than in large cerebral infarction, so
greater risk of herniation and death
In chronic phase, prognosis for surviving
patients much better than with ischemic
stroke

Subarachnoid Hemorrhage

Aneurysms can rupture any time but more


common during strenuous activity
Most common manifestation is headache
worst headache of my life
Neck pain and rigidity
Loss of consciousness and vomiting common
Seen on CT in 95% of cases location may
suggest site of rupture
Normal CT does not rule out so do lumbar
puncture xanthochromia (develops after 6
hours)

Causes of Spontaneous
Intracerebral Hemorrhage
(ICH)

Subarachnoid hemorrhage
Congenital saccular aneurysm (85%)
Unknown (15%)

What Parts of the Brain


Are Affected by Stroke?

Right (Non-dominant)
Hemisphere Stroke:
Common Pattern

Neglect of left visual field


Extinction of left-sided stimuli
Left hemiparesis
Left-sided sensory loss
Left visual field defect
Poor left conjugate gaze
Dysarthria
Spatial disorientation

Left (Dominant)
Hemisphere Stroke:
Common Pattern

Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Poor right conjugate gaze
Dysarthria
Difficulty reading, writing, or
calculating

Brain Stem / Cerebellum /


Posterior Hemisphere Stroke:
Common Pattern
Motor or sensory loss in all four limbs

Crossed signs
Limb or gait ataxia
Dysarthria
Dysconjugate gaze
Nystagmus
Amnesia
Bilateral visual field defects

Small Subcortical
Hemisphere or Brain Stem
Stroke:
Common
Pattern

Pure Motor

Weakness of face and limbs on one side of the


body without abnormalities of higher brain
function, sensation, or vision

Pure Sensory
Decreased sensation of face and limbs on one
side of the body without abnormalities of
higher brain function, motor function, or vision

Physical Exam
Neurologic Exam
Carotid Bruits
Cardiac Exam
Peripheral Pulses
Dermatologic
Ophthalmologic

Dermatologic

Splinter hemorrhages and needle


tracks (endocarditis)
Xanthoma (hyperlipidemia)
Caf-au-lait spots
Neurofibromas (neurofibromatosis)
Purpura (coagulopathy)
Capillary angiomata (cavernous
malformation)

Xanthoma, eruptive
CAF AU LAIT spots

Neurofibromas
splinter hemorrhages

Opthalmlogic

Corneal arcus (hypercholesterolemia)


Corneal opacity (Fabrys disease)
Lisch nodules
Optic atrophy (neurofibromatosis)
Lens subluxation (Marfans syndrome,
homocystinuria)
Retinal perivasculitis (sickle-cell disease, syphilis,
connective tissue diseases, inflammatory bowel
disease)
Occlusions (emboli)
Angioma (cavernous malformation)
Hamartoma (tuberous sclerosis).

Corneal arcus
optic atrophy in tuberous sclerosis

lens dislocation in marfan syndrome

Diagnostic Testing for Patients


With Stroke

Basic stroke evaluation


Cranial computed tomography (CT)
Carotid ultrasonography transcranial Doppler
Transthoracic echocardiography
EKG monitoring
Routine blood studies (complete blood count with
differential and platelet count, prothrombin time
(international normalized ratio), activated partial
thromboplastin time, glucose, chemistries,
serology for syphilis, and an erythrocyte
sedimentation rate)

Diagnostic Testing for Patients


With Stroke

Comprehensive stroke evaluation


Cranial magnetic resonance imaging (MRI)
Imaging of the intracranial arteries (MR, CT, or catheter angiography
of the brain)
Imaging of the extracranial arteries (MR, CT, or catheter angiography
of the neck)
Transesophageal echocardiography (TEE)
Prolonged EKG monitoring with Holter or event loop recorder
Urine toxicology screen (often productive)
Urine pregnancy test
Blood testing for a hypercoagulable state anticardiolipin antibodies, lupus
anticoagulants, protein S, protein C, activated protein C resistance,
antithrombin III) is requested in patients without a firmly identified cause
of stroke or if the patient or family members have a history of thromboses.
It is advantageous to send such a profile prior to initiating anticoagulation,
as heparin can alter interpretation of some of those assays.
In select cases, blood testing for rare genetic causes of stroke (CADASIL,
Fabry disease, MELAS)

How Are Strokes Treated?


Ischemic Stroke
Clot-busters e.g., t-PA
Anticoagulants warfarin, aspirin
Carotid Endarterectomy
Angioplasty/Stents

Treatment of Strokes
Antiplatelet therapy remains treatment
of choice to prevent recurrent
thromboembolism in majority of
patients
Anticoagulation may be appropriate
Atrial fibrillation
Recent MI
Suspected propagation of thrombus or
stroke in evolution

Treatment of Strokes

CT or MRI of the brain should be


performed promptly; MRI is more
sensitive for early ischemic changes,
but either method can fully rule out
hemorrhage.
Treatment of TPA was associated
with an increase of about 1.2 with
minimal or no disability for every 10
patients treated.

Limitations of Imaging

CT will miss a minority of acute


bleeds
MRI with DWI (diffusion weighted
imaging), quite sensitive for acute
stroke, has an occasional false
negative result (17 out of 782
patients in a recent study)
MRAs resolution is not yet on par
with conventional angiography.

Thrombolysis t-PA
Guidelines for treatment:

Present within 3 hours of onset of clearly


defined stroke frequency of symptomatic
hemorrhage most likely increases after this
time

CT scan shows no evidence of


intracranial hemorrhage
No anticoagulants or antiplatelet agents
given for 24 hours
Avoid BP values > 185/110

Guidelines Not to Treat


Previous stroke or serious head
trauma in preceding 3 months
History of intracranial hemorrhage
Repeated systolic BPs > 185 mm Hg
or diastolic BPs > 110 mm Hg

Guidelines Not to Treat


Requires aggressive treatment to
reduce BP to specified limits
Taking anticoagulants or propensity to
hemorrhage
Recent invasive surgical procedure
Rapidly improving neurological deficit
or minor symptoms

How Are Strokes Treated


Hemorrhagic Stroke
Surgical Intervention
Endovascular Procedures, e.g.,
coils

What Is the Impact of Stroke?


Stroke is the third leading cause of
death in the United States
On average, someone suffers a
stroke every 40 seconds
About 795,000 Americans suffer a
stroke each year
About every 4 minutes, someone
dies of a stroke

What Is the Impact of Stroke?

Stroke is a leading cause of serious,


long term disability
About 6.4 million Americans are
stroke survivors
Americans will pay about $73.7
billion in 2010 for stroke-related
medical costs and lost productivity
long-term

Rehabilitation

After suffering a stroke, its


important to begin a rehabilitation
program as soon as possible.
Types of rehabilitation programs:
Hospital programs
Extended care facilities
Outpatient programs
Home-based programs

Rehabilitation Specialists

Provider
Rehabilitation specialist
Physical therapist
Speech therapist
Occupational therapist
Physiatrist
Psychiatrist

Family Relationships

Overall, 13 studies reported consequences of


stroke for family relationships and in those
studies, 5% to 54% of the samples experienced
family problems.
Nine studies reported marital problems after
stroke, including separation or divorce.
Six of these reported that marital problems were
a direct consequence of the stroke.
One study reported that 5% of the sample had
experienced deterioration in the spousal
relationship, whereas another found that 38% of
couples had experienced conflict since the stroke.

Sexual Relationships

Ten studies investigated the impact


of stroke on sexual relationships,
reporting problems in participants
sexual relationships or frequency of
sexual activities.
Prevalence of deterioration in sexual
relationships reported in 8 studies
ranged from 5% to 76%.

Social Activities

Nine studies reported consequences


of stroke on social or leisure
activities with 4 of these reporting
deterioration or decrease in these
activities.
Five studies quantified reported
decrease in leisure activities ranging
from 15% to 79%.

Prognosis

The outcome of stroke in young adults is better than that


for older adults. In a recent study of 330 patients with first
stroke or transient ischemic attack, followed for an average
of 96 months, 8% died, 3% had another stroke, and 3%
had a myocardial infarction. Approximately 16% were
dependent, but 56% had returned to work. Unfortunately,
only a minority of those who smoked at the time of their
stroke subsequently stopped using tobacco. The overall
annual recurrence rate is less than 1%.
Prognosis is often closely associated with the underlying
cause.
A relatively good outcome may be found after many cases
of arterial dissection.
Risk of stroke recurrence is low (2% over 5 years) in
women whose first stroke occurred in pregnancy.

Stroke Chameleons

Strokes with atypical presentations that take on


the appearance of other disease process may be
termed stroke chameleons, for like the
chameleon, these disguised strokes may change
and evolve with time.
The provider is left with the daunting problem of
discovering the unusual manifestation of an
uncommon clinical process.
The presence of historical risk factors for
cerebrovascular disease and the abrupt onset of
symptoms may be the best clues available to the
provider to detect these unusual stroke
syndromes.

Stroke Chameleons

In the majority of cases of stroke, making


the diagnosis is straightforward.
Especially in patients with unusual
features (e.g.,
Gradual onset,
Seizure at the onset of symptoms
Impaired consciousness
The differential diagnosis should include
migraine, postictal paresis, hypoglycemia,
conversion disorder, subdural hematoma,
and brain tumors.

Stroke Chameleons

Atherosclerosis (leading to thromboembolism or


local occlusion) and cardioembolism are the
leading causes of brain ischemia.
Unusual causes should be considered, especially if
patients are younger (e.g., below 50 years of age)
and have no apparent cardiovascular risk factors.
Some clinical clues that suggest alternative
diagnoses are ptosis and miosis contralateral to
the deficit (carotid-artery dissection), fever and a
cardiac murmur (infective endocarditis), and
headache and an elevated erythrocyte
sedimentation rate.

Differential
Diagnosis

Seizures and migraine auras


characteristically (but not always) begin
with positive symptoms, while TIAs
invariably are characterized by negative
symptoms.
Seizures occasionally cause paralytic
attacks but, on close observation, there
are usually features of the history and
physical examination that suggest the
presence of a seizure disorder such as
minor twitching of a finger or toe or a
tingling sensation in the affected limb.

Differential Diagnosis of Stroke

Intracranial mass: Tumor, Subdural


hematoma
Seizure with persistent neurological
signs
Migraine with persistent neurological
signs
Metabolic

Differential Diagnosis of Stroke

Hyperglycemia (nonketotic
hyperosmolar coma)
Hypoglycemia
Post-cardiac arrest ischemia
Drug/narcotic overdose

Focal
symptom
s

Nonfocal
symptoms

Seizures

++

++

TIAs

++++

occasionally

Migraine

++++

++++

Common
disorders

Syncope

Less common
disorders
Vestibulopathy

++

++

Metabolic

+++

"Tumor attacks"

+++

Multiple
sclerosis

++++

Psychiatric

++

Nerves and
nerve root

++++

Transient global
amnesia

++++

0
++

Differential
Diagnosis of Transient Neurological
Diseases

TIA
Seizure
Migraine with aura
Syncope
Hypoglycemia

Hypoglycemia

That transient hypoglycemia may produce a stroke like picture


with hemiplegia and aphasia has been known for years.
These patients may be drowsy but are often alert and do not show
the more common response to hypoglycemia of confusion,
diminished level of consciousness, or coma.
Aphasia may make the history of diabetes more difficult to
discover.
Syndrome has also been reported in alcoholics with hypoglycemia.
The pathogenesis of this focal CNS dysfunction is unclear.
Hypoglycemia is generally defined as a blood glucose level of less
than 45 mg/dl in these studies.
The wide use of bedside rapid laboratory testing for glucose now
makes this easily detectable and treatable.
The hemiplegia may resolve immediately with the administration
of intravenous glucose but resolution over a hours is also
reported.

Mass Lesions

Subdural hematoma, cerebral abscess, primary CNS


tumors, and metastatic tumors are among the clinical
conditions simulating stroke in the studies cited above.
The typical clinical presentation of a slowly increasing mass
is a progressive syndrome; an abrupt onset of symptoms of
these masses seems counter-intuitive.
A review of patients with brain tumors presenting to an ED
showed that 6% of patients had symptoms that were of less
than one days duration; it was thought that these patients
with brief symptom duration might reflect a sub-population
who suffer acute deterioration from hemorrhage into the
tumor or who develop obstructive hydrocephalus.
Secondary effects of mass or edema on cerebral vasculature
have been identified as possible causes of abrupt onset of
seizures as well.
Chronic subdural hematoma has been frequently reported
as a cause of stroke and TIA-like symptoms.

Functional Hemiparesis

Little is written about a factitious or feigned stroke yet


several studies discover rare patients initially thought to
have cerebrovascular disease but later determined to have
a functional cause of the hemiparesis or other stroke
syndrome.
Conversion disorder is the most commonly assigned
psychiatric disorder.
One study of emergency department presentations of
conversion disorder noted that symptoms of paresis,
paralysis, or movement disorders were common and were a
presentation in almost 30% of patients.
They noted significant comorbidity in this population, often
other psychiatric disorders, and emphasized that
conversion disorder is a diagnosis of exclusion.
Patients often undergo multiple diagnostic tests before the
diagnosis is assigned.

Seizures Demographics

Any age, often younger

Seizures CNS Symptoms

Light-headed, dim vision, noises


distant, decreased alertness
Transient loss of consciousness

Seizures CNS Symptoms

Positive symptoms: limb jerking,


head turning, loss of consciousness
Negative symptoms may develop,
remain postictally, and persist

Seizures Timing

20 to 80 seconds
Absence, atonic seizures and
myoclonic jerks are shorter
Postictal depression
Spells occur over years

Seizures Associated Symptoms

Tongue biting, incontinence, sore


muscles, headache after attack

Focal Seizure

Partial (focal) seizure


Positive sensory or motor symptoms
Spread quickly (60 seconds)
Negative symptoms afterward (Todds
paresis)
Multiple attacks

What is a TIA
Acute loss of focal cerebral function
Symptoms last less than 24 hours
Due to inadequate blood supply
Thrombosis
Embolism

Transient Ischemic Attacks (TIAs)

Warning strokes that can happen before a major


stroke
Occur when blood flow through a brain artery is
blocked or reduced for a short time
Symptoms are temporary (<24 hours) but similar
to those of a full fledged stroke
A person who has a TIA is 9.5 times more likely
to have a stroke

TIA Risk Factors/Epidemiology

300,000 TIAs per year in US


5-year stroke risk after TIA 29%
43.5% in 2 years with >70% carotid stenosis
treated medically

Many stroke patients have had a TIA


25% - 50% in large artery atherothrombotic
strokes
11% - 30% in cardioembolic strokes
11% to 14% in lacunar strokes

Risk Factors for a TIA

Risk factors are the same as stroke

Increasing age
Sex
Family history / Race
Prior stroke / TIA
Hypertension
Diabetes
Heart disease
Carotid artery / Peripheral artery disease
Obesity
High cholesterol
Physical inactivity

TIA Symptoms

Symptoms last less than 24 hours


Most last less than one hour
Less than 10 percent > 6 hours
Amaurosis fugax up to five minutes
(Amaurosis fugax is loss of vision in
one eye due to a temporary lack
of blood flow to the retina. Symptoms
include the sudden loss of vision in one
eye.)

TIA Demography

Older patients
Stroke risk factors present
Men>women

TIA Presentation

Acute loss of focal cerebral function


Abrupt onset
Symptoms occur in all affected areas at
the same time
Symptoms resolve gradually
Symptoms are negative

TIA Presentation

Acute loss of focal cerebral function


Motor symptoms
Weakness or clumsiness on one side
Difficulty swallowing
Speech disturbances
Understanding or expressing spoken
language
Reading or writing
Slurred speech
Calculations

TIA Presentation

Acute loss of focal cerebral function


Sensory symptoms
Altered feeling on one side
Loss of vision on one side
Loss of vision in left or right visual field
Bilateral blindness
Double vision
Vertigo

TIA Presentation

Non-focal Symptoms (Not TIA)


Generalized weakness or numbness
Faintness or syncope
Incontinence
Isolated symptoms (symptoms
occurring alone)
Vertigo or loss of balance
Slurred speech or difficulty swallowing
Double vision

TIA Presentation

Non-focal Symptoms (Not TIA)


Confusion

Disorientation
Impaired attention/concentration
Diminution of all mental activity
Distinguish from
Isolated language or visual-spatial perception
problems (may be TIA)
Isolated memory problems (transient global
amnesia)

TIA
Significant risk factor for recurrent
stroke, with average 5% risk per year
Prophylactic antiplatelet therapy shown
to prevent secondary effects
Aspirin
Ticlopidine: thrombotic stroke
reduction
Clopidogrel: reduce events associated
with atherosclerosis that include
strokes, MI, PVD

TIA
Treat with warfarin if significant risk for
cardiogenic thromboembolism
Hospital admission for new-onset and
recurrent TIAs unless confident in
diagnosis of etiology
Angiography treat medically or
surgically

TIA

Usually minutes, mostly <1 hour


Spells during days, weeks, months;
not usually years

TIA Associated Symptoms

Headaches may occur during time


period of a TIA

Migraine Demography

Younger age
Women>men (4:1)
10-20% of the population
The risk of migraine with aura and
transient ischemic attacks (TIAs) is
greater than 2 fold.
1/3 have migraine with aura

Migraine with Aura

Migraine with aura

Positive symptoms
Spread over minutes
Visual disturbances
Somatosensory or motor disturbance
Headache within 1 hour

Migraine with aura is associated with a


twofold risk of ischemic stroke. This risk is
higher in women, age < 45, smokers, and
women who used oral contraceptives.
BMJ2009;339:b3914, Migraine and cardiovascular disease

Migraine with Aura

Aura without Headache


98%
30%

Visual symptoms
with other symptoms

26% sensory
16% aphasia
6% dysarthria
10% weakness

Mean age 48.7 (vs. 62.1)


Fewer cardiovascular risk factors

Migraine CNS Timing

Usually 20 to 30 minutes
Sporadic attacks during years

Migraine with Aura

Migraine Associated Symptoms

Headache after attack, nausea,


vomiting, photophobia, phonophobia
(usually GI or autonomic nervous
system)

Migraine

Auras typically occur before the onset of


migraine headache, and the headache
usually begins simultaneously with or just
after the end of the aura phase. However,
headache onset can rarely occur an hour
or more after the end of the aura phase.
Although atypical, an aura can develop
during or after the onset of headache, and
many patients have migraine aura with
only a minimal or no headache.

Migraine

Most migraine auras resolve in 20 to 30


minutes and seldom last more than one
hour.
Typical auras may involve any of the
following manifestations:
Visual disturbances ( the most common
type of aura)
Sensory symptoms
Motor weakness
Speech disturbances

Migraine vs. TIA

Positive visual symptoms


Gradual onset / evolution
Sequential progression
Repetitive attacks of
identical nature
Flurry of attacks mid-life
Duration up to 60 minutes
Headache follows ~ 50%

Visual loss
Abrupt
Simultaneous occurrence

Duration <15 minutes


Headache uncommon
accompaniment

Syncope Demography

Any age, often younger


Women>men

Syncope Timing

Usually a few seconds


Sporadic attacks during years

Syncope Associated Symptoms

Sweating, pallor, nausea

Most Common Types of Syncope

Neurocardiogenic (vasovagal) syncope


Situational syncope (during or
immediately after urination,
defecation, cough, or swallowing)
Orthostatic syncope (associated with
orthostatic hypotension)
Syncope related to cardiac ischemia or
cardiac arrhythmia

Differential diagnosis of transient neurologic symptoms

Seizures
Demography

Any age, often


younger

TIAs

Migraine

Syncope

Older patients

Younger age

Any age, often


younger

Stroke risk factors


present

Women>men

Women>men

First positive
symptoms, then
negative in same
modality: scintillating
scotomas and
parasthesias most
common; second
sensory modality is
involved after first
clears

Light-headed, dim
vision, noises
distant, decreased
alertness

Men>women
Central nervous
system symptoms

Timing

Positive symptoms:
limb jerking, head
turning, loss of
consciousness

Negative symptoms:
numbness, visual
loss, paralysis, ataxia

Negative symptoms
may develop, remain
postictally, and
persist

All sensory
modalities affected
simultaneously

20 to 80 seconds

Usually minutes,
mostly <1 hour

Usually 20 to 30
minutes

Usually a few
seconds

Absence, atonic
seizures and
myoclonic jerks are
shorter

Spells during days,


weeks, months; not
usually years

Sporadic attacks
during years

Sporadic attacks
during years

Postictal depression
Spells occur during
years

Transient loss of
consciousness

Transient Global Amnesia


Sudden disorder of memory
Antegrade and often retrograde
Recurrence 3% per year
Etiology unclear
Migraine
Epilepsy (7% within 1 year)
Unknown

Transient Global Amnesia


No difference in vascular risk factors
compared with general population
Fewer risk factors when compared with
TIA patients
Prognosis significantly better than TIA

Structural intracranial lesion


Tumor
Partial seizures
Vascular steal
Hemorrhage
Vessel compression by tumor

Intracranial hemorrhage
ICH rare to confuse with TIA
Subdural hematoma
Headache
Fluctuation of symptoms
Mental status changes

Multiple sclerosis
Usually subacute but can be acute
Optic neuritis
Limb ataxia

Age and risk factors


Signs more pronounced than symptoms

Labyrinthine Disorders
Central vs. Peripheral vertigo
Mnire's disease
Benign positional vertigo
Acute vestibular neuronitis

Others in the Differential Diagnosis

Metabolic perturbations, such as


hypoglycemia, can be associated with focal
neurologic deficits.
Multiple sclerosis occasionally can cause
paroxysmal attacks, particularly of ataxia
and dysarthria.
Brain tumors can occasionally result in
transient neurologic symptoms; the
mechanism in these cases is thought to
involve mechanical changes that result in
pressure on structures adjacent to the
tumor.

Others in the Differential Diagnosis

Subdural hematomas may cause attacks of


transient neurologic dysfunction, again due to
mechanical changes that result in pressure on
structures adjacent to the hematoma.
Cerebral amyloid angiopathy, better known as a
cause of intracerebral hemorrhage, may also
cause transient neurologic symptoms. Affected
patients complain of recurrent, brief (minutes),
often stereotyped spells of weakness, numbness,
paresthesias, or other cortical symptoms that can
spread smoothly over contiguous body parts.

Others in the Differential Diagnosis

Hepatic, renal, and pulmonary


encephalopathies can produce temporary
aberrations in alertness, behavior and
movement.
Compressive myelopathy may rarely cause
sudden transient sensory changes and
motor deficits.
Pressure- or position-related peripheral
nerve or nerve root compression can cause
transient paresthesias and numbness.

Others in the Differential Diagnosis

Peripheral vestibulopathies can cause


transient episodic dizziness.
Hysteria and other psychiatric
disorders may underlie attacks that
include swoons, falls, and episodic
blindness, deafness, and paralysis,
which can be confused with organic
loss of function.

Case 1

A 19 year old man had a history of a


murmur since birth and intermittent
episodes of hemiparesis that he
ignored. He presented with collapse
while playing handball.

Case 1

He fell and had tonic clonic movement of


his extremities. He was in distress at
presentation
His BP was 110/70, HR 76, RR 18. He had
a persistently split S2 with a systolic
ejection murmur in the upper left second
intercostal area. His neurological exam
was consistent with a right middle cerebral
infarction with a left hemiplegia and left
hemisensory defect.

Case 2
When 22-year-old Ms. KS began
experiencing left arm weakness, she
went to a clinic only to be told that
nothing was seriously wrong. But
when her symptoms persisted, so did
she. She was finally referred to the
Medical Center, where neurologists
confirmed that her symptoms were
the result of a stroke.

Case 2

Further testing in the Coagulation


Laboratory revealed activated protein
C resistance, the result of a
heterozygous mutation in factor V
Leiden, as well as a homozygous
mutation in the methylene
tetrahydrofolate reductase gene,
responsible for elevated homocystine

Case 2

Although she had had only one clinical stroke,


multiple other strokes were evident by imaging
studies. Factors contributing to her
hypercoagulable state included: 1. the methylene
tetrahydrofolate reductase deficiency, which
elevated her homocystine level, 2. the
heterozygous state for factor V Leiden, causing
activated protein C resistance, 3. oral
contraceptives, 4. smoking, and 5. hypertension.
She is doing well, without recurrence, on aspirin,
and antihypertensive medicines, having stopped
smoking and birth control pills.

Case 3

In another case, a 20-year-old female


college student was sent to the Medical
Center after a brain scan showed what her
physicians thought to be a brain tumor.
Neurosurgeons quickly realized there was
no tumor, and that the young woman had
suffered a stroke. After thrombosis of
intracranial venous sinuses was diagnosed
she was treated with heparin, and then
Warfarin. Repeat imaging revealed
recanalization of the previously
thrombosed sinuses.

Case 3

Investigation in the Special Coagulation


Laboratory revealed deficiency of
antithrombin III, on two separate
occasions, several weeks apart. This
patient suffered a venous infarction
secondary to a hypercoagulable state
induced by inherited antithrombin III
deficiency, probably exacerbated by use of
oral contraceptives. With anticoagulation
and careful monitoring, her prognosis is
good.

Case 4

A 28-year-old man has sudden weakness of the left


arm and leg and slurred speech.
Except for untreated hypertension, his medical
history is unremarkable.
He is a current smoker.
On arrival at the emergency department 1 hour 15
minutes after the onset of symptoms, he reports no
headache or vomiting.
His blood pressure is 180/100 mm Hg, and his pulse
is 76 beats per minute and is regular.
Neurologic examination shows dysarthria, a left
homonymous hemianopia, severe left-sided
weakness, and a failure to register light touch on the
left side of the body when both sides are touched
simultaneously (left tactile extinction).

Case 4

He had sudden left-sided


hemiparesis, strongly suggestive of a
right hemisphere stroke.

Summary

These are not isolated cases. Frequently


young patients, even teenagers, who have
suffered stroke are misdiagnosed. Though
they may have presented with classic
symptoms - dizziness, severe headache,
weakness in a limb, or unilateral loss of
sensation, for example - they often have
been misdiagnosed by their provider, most
likely because they do not fit the profile of
the "typical" stroke patient.

Summary

Misdiagnosis has included patients


being told they had vertigo,
migraine, alcohol intoxication or
other conditions. They were
discharged from clinic and later
discovered to have suffered a stroke.

Summary

The second important point is that the


causes of stroke in young people are much
more diverse, and less likely to be the
ones that commonly cause stroke in older
people, such as atherosclerosis of brainsupplying vessels and emboli from cardiac
disorders related to coronary artery
disease. Without the right resources,
providers may be at a loss to pinpoint the
cause in order to treat it and prevent
further damage.

Summary

Abuse of amphetamine-like drugs


("speed" and cocaine, for example)
can lead to stroke in teenagers and
young adults. These drugs are
popular in rural and urban areas
alike.

Summary

However, one of the increasingly


recognized causes of stroke in a young
person is a blood disorder that predisposes
to blood clotting.This allows clots to form
too readily, often in the veins, leading to
stroke. Once such a disorder has been
identified, treatment can help prevent
future damage. Diagnosis of a hereditary
disorder can also lead to identification of
other family members who may be at high
risk.

Summary

The long term outcome of cerebral


infarction is better in young adults
than in older patients, morbidity and
mortality are still significant.
Despite a good functional and motor
outcome young adult patients usually
encounter difficulties in social and
work caused by cognitive
impairment.

Summary

The bottom line: for young stroke


patients, extensive testing and
careful evaluation may be necessary
to determine the underlying cause.

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