Stroke Syndromes
Dr. Gerrard Uy
Cerebrovascular Disease
• ischemic stroke
• hemorrhagic stroke
• cerebrovascular anomalies such as intracranial
aneurysms and arteriovenous malformations
(AVMs)
• Cause 200,000 deaths each year in the U.S.
• Incidence increases with age
Stroke
• Most strokes manifest by the abrupt onset of
a focal neurologic deficit
• Like patients were “struck by the hand of God”
• Definition:
• abrupt onset of a neurologic deficit that is
attributable to a focal vascular cause
Definition of terms
• Thrombosis: inappropriate clotting
• Embolism: migration of clots
• Ischemia: loss of blood supply in a tissue due
to impeded arterial flow or reduced venous
drainage
• Infarction: cell death
Definition of Terms
• Cerebral ischemia is caused by a reduction in
blood flow that lasts longer than several
seconds
• infarction - death of brain tissue
• transient ischemic attack (TIA) - all neurologic
signs and symptoms resolve within 24 h
regardless of whether there is imaging
evidence of new permanent brain injury
Hemorrhagic Stroke
• Bleeding into subdural and epidural spaces is
principally produced by trauma
• SAHs are produced by trauma and rupture of
intracranial aneurysms
• Hemorrhage are classified by location
• Often identified by CT scan
Approach to the patient
• Rapid evaluation is essential for use of time
sensitive treatments such as thrombolysis
• Most patients with acute stroke do not seek
medical attention because they are rarely in pain
and they experience anosagnosia
• Important clues pointing to stroke:
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Hemiparesis
Changes in vision
Changes in gait
Disturbance in the ability to speak or understand
Sudden severe headache
Approach to the patient
• Migraine can mimic stroke
• The sensory and motor deficit tend to migrate
slowly across a limb over minutes rather than
seconds as with stroke
• Once diagnosis of stroke is made, brain
imaging study is necessary to determine the
cause of the stroke whether ischemic or
hemorrhagic
• CT imaging is the standard imaging procedure
ISCHEMIC STROKE
Ischemic Stroke
• Acute occlusion of an intracranial vessel causing
reduction in blood flow to the brain region
• The magnitude of flow reduction is a function of
collateral blood flow
• INFARCTION results when:
– Cerebral blood flow of 0 (zero) in 4 – 10 mins
– CBF <16-18 ml/ 100g tissue per min in 1 hour
• CBF <20ml/100g tissue per min = ischemia
• The tissue surrounding the infarction is ischemic
and is called the ischemic penumbra
Pathophysiology
• Ischemia produces necrosis by starving
neurons of glucose
• No glucose means no ATP production
• No ATP, the neurons start to depolarize which
in turn increases intracellular calcium levels to
rise and glutamate to accumulate
• Free radicals produced in this process will
result in cellular dysfunction and death
Management of Acute Ischemic Stroke
• First goal is to prevent or reverse brain injury
• Check ABCs and treat hypoglycemia or
hyperglycemia
• Brain imaging to determine whether stroke is
ischemic or hemorrhagic
Management of Acute Ischemic Stroke
• 6 categories to improve clinical outcome
– Medical support
– Intravenous thrombolysis
– Endovascular techniques
– Antithrombotic treatment
– Neuroprotection
– rehabilitation
Management of Acute Ischemic Stroke
• Medical Support
– Immediate goal is to optimize cerebral perfusion
– Prevent complications such as infections, DVT, and
bedsores
– Maintain euglycemia
– Treat fever
– Manage hypertension
– Use of IV Mannitol to raise serum osmolarity and
prevent brain edema
Management of Acute Ischemic Stroke
• Intravenous Thrombolysis:
– NINDS rTPA stoke study showed benefit for IV
rTPA in selected patients with acute stroke
– Golden period is within 3 hrs of the onset of
ischemic stroke (0.9 mg/kg – 10% as bolus and
remainder over 1 hr)
– The time of onset of stroke is defined as the time
patient’s symptoms began or the time the patient
was last seen normal
Management of Acute Ischemic Stroke
• Indications for rTPA
– Clinical diagnosis of stroke
– Onset < 3 hrs
– CT scan shows no hemorrhage or edema of > 1/3
of the MCA territory
– Age > 18 yrs of age
– consent
Management of Acute Ischemic Stroke
• Contraindications
– Sustained BP > 185/110 despite treatment
– Plt < 100,000, hct < 25%, glucose <50 or >400 mg/dl
– Use of heparin within 48 hrs, prolonged PTT, or elevated
INR
– Rapidly improving symptoms
– Prior stroke or head injury within 3 months
– Major surgery in preceding 14 days
– Minor stroke symptoms
– GI bleeding in preceding 21 days
– Recent MI
– Coma or Stupor
Management of Acute Ischemic Stroke
• Endovascular Techniques
– Usually done in occlusions of large vessels such as
MCA, internal carotid artery, and basilar artery
– Procedure is done intraarterially
– Mechanical thrombectomy is an alternative
Management of Acute Ischemic Stroke
• Antithrombotic Treatment
– Platelet inhibition
• Aspirin is the only antiplatelet agent that has been
proven effective for the acute treatment of ischemic
stroke
• Usually given within 48 hrs of stroke onset
– Anticoagulation
• Has shown no benefit in the primary treatment of
atherothrombotic cerebral ischemia
Management of Acute Ischemic Stroke
• Neuroprotection
– To provide a treatment that prolongs the brain’s
tolerance to ischemia
– Most common neuroprotective drug:
• Citicoline – reduces the rate of death and disability
Management of Acute Ischemic Stroke
• Rehabilitation
– to improve neurologic outcomes and reduce
mortality
– Directed towards educating the patient and family
about the patient’s neurologic deficit, preventing
complications of immobility and providing
encouragement and instruction in overcoming the
deficit
– Goal is to return the patient home and to
maximize recovery
Causes of Ischemic Stroke
• establishing a cause is essential in reducing
the risk of recurrence
• 30% of strokes remain unexplained despite
extensive evaluation
• Focus on: atrial fibrillation and carotid
atherosclerosis
Causes of Ischemic Stroke
Cardioembolic Stroke
• Responsible for 20% of all ischemic strokes
• embolism of thrombotic material forming on
the atrial or ventricular wall or the left heart
valves
• thrombi then detach and embolize into the
arterial circulation
• Embolic strokes tend to be sudden in onset,
with maximum neurologic deficit at once
Cardioembolic Stroke
• Emboli from the heart most often lodge in the
MCA, PCA, and infrequently ACA
• Nonrheumatic atrial fibrillation is the most
common cause of cerebral embolism overall
• Patient’s with atrial fibrillation have an
average annual risk of 5%
• Left atrial enlargement and CHF are additional
risk factors for the formation of atrial thrombi
Cardioembolic Stroke causes:
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nonrheumatic atrial fibrillation
MI
prosthetic valves
rheumatic heart disease
ischemic cardiomyopathy
Carotid Atherosclerosis
• 10% of all ischemic strokes
• frequently within the common carotid
bifurcation and proximal internal carotid
artery
• RISK FACTORS:
– Male gender, older age, smoking, hypertension,
diabetes, and hypercholesterolemia
Other causes of stroke
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Intracranial Atherosclerosis
Dissection of Internal Carotid Artery
Hypercoagulability
Venous sinus thrombosis
Fibromuscular dysplasia
Vasculitis
Drugs (amphetamines, cocaine,
phenylpropanolamine)
Transient Ischemic Attack (TIA)
• Episodes of stroke symptoms that last briefly
• Duration < 24 hrs
• May arise from emboli to the brain or from in
situ thrombosis
• Amaurosis fugax – transient monocular
blindness occurs from emboli to the central
retinal artery of the eye
Transient Ischemic Attack (TIA)
• Risk of stroke after a TIA is ~10-15% in the first 3
months with most events occurring in the first 2
days
• Acute antiplatelet therapy is effective and
recommended
• Atherosclerotic risk factors:
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Old age
Family history of thrombotic stroke
DM
Tobacco smoking
dyslipidemia
Transient Ischemic Attack (TIA)
• Other risk factors:
– Prior stroke or TIA
– Certain cardiac conditions
– Oral contraceptives
– Hypertension – most significant risk factor
Transient Ischemic Attack (TIA)
Treatment
• Antiplatelet agents
– Aspirin:
• Can prevent platelet aggregation
• Acetylates cyclooxygenase whicg irreversibly inhibits
the formation in platelets of thromboxane A2
• Effect is permament and lasts for the usual 8-day life of
the platelet
• Also inhibits endothelial prostacyclin, and
antiaggregating and vasodilating prostaglandin
• 50-325 mg/day is recommended for stroke prevention
Transient Ischemic Attack (TIA)
Treatment
• Antiplatelet agents
– Clopidogrel:
• Blocks the ADP receptor on platelets blocking the
platelet aggregation
– Dypiridamole:
• Inhibits the uptake of adenosine by a variety of cells
• Adenosine = inhibitor of aggregation
• Also potentiates the anti aggregatory effects of
prostacyclin and nitric oxide by inhibiting platelet
phosphodiesterase
• Prinicpal side effect is headache
Transient Ischemic Attack (TIA)
Treatment
• Anticoagulation therapies
– The decision to use anticoagulation for primary
prevention is based on risk factors (rheumatic
heart disease, atrial fibrillation, and prosthetic
valve implantation)
STROKE SYNDROMES
Middle Cerebral Artery
Middle Cerebral Artery
• entire MCA is occluded at its origin :
– contralateral hemiplegia,
hemianesthesia, homonymous
hemianopia, and a day or two of gaze
preference to the ipsilateral side
– Dysarthria is common because of
facial weakness
– global aphasia
– anosognosia, constructional apraxia,
and neglect