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stroke 1

A cerebrovascular accident (CVA), or stroke, occurs due to disrupted blood flow to the brain, primarily classified as ischemic or hemorrhagic. Symptoms include sudden weakness, difficulty speaking, and severe headache, necessitating immediate medical attention as stroke is a leading cause of death globally. Understanding stroke syndromes, diagnostic imaging, and the pathophysiology of ischemic stroke is crucial for effective treatment and improving patient outcomes.

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0% found this document useful (0 votes)
7 views69 pages

stroke 1

A cerebrovascular accident (CVA), or stroke, occurs due to disrupted blood flow to the brain, primarily classified as ischemic or hemorrhagic. Symptoms include sudden weakness, difficulty speaking, and severe headache, necessitating immediate medical attention as stroke is a leading cause of death globally. Understanding stroke syndromes, diagnostic imaging, and the pathophysiology of ischemic stroke is crucial for effective treatment and improving patient outcomes.

Uploaded by

dryahyeone
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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• A cerebrovascular accident (CVA), commonly known as a stroke, is a

medical condition that occurs when there is a disruption of blood flow


to the brain. This can happen in two primary ways:

• Ischemic Stroke: This is the most common type, accounting for about 87% of
strokes. It occurs when a blood vessel supplying blood to the brain is
obstructed, often due to a blood clot or plaque buildup in the arteries.
• Hemorrhagic Stroke: This type occurs when a blood vessel in the brain
ruptures, leading to bleeding in or around the brain. It can be caused by
conditions such as high blood pressure or aneurysms.
• Symptoms of a CVA can include sudden weakness or numbness,
difficulty speaking or understanding speech, vision problems, loss of
balance, and severe headache. Immediate medical attention is crucial,
as prompt treatment can significantly improve outcomes and reduce
the risk of long-term disability.
• Stroke is the second leading cause of death worldwide, with 6.2
million dying from stroke in 2015, an increase of 830,000 since the
year 2000. In 2016, the lifetime global risk of stroke from age 25 years
onward was 25%, an increase of 8.9% from 1990. Nearly 7 million
Americans age 20 or older report having had a stroke, and the
prevalence is estimated to rise by 3.4 million adults in the next
decade, representing 4% of the entire adult population.
Transient Ischemic Attack (TIA)

• A Transient Ischemic Attack (TIA) is a temporary episode of neurological


dysfunction caused by a brief interruption in blood flow to the brain. Here are
key points about TIA:
• Characteristics
• Duration: Symptoms typically last for a few minutes to less than 24 hours but
generally resolve completely within an hour.
• Symptoms: Can mimic those of a stroke and may include:
• Sudden weakness or numbness in the face, arm, or leg, especially on one side of the
body
• Difficulty speaking or understanding speech
• Vision problems, such as blurred or double vision
• Dizziness, loss of balance, or coordination issues
Approach to the Patient with Cerebrovascular
Disease

• When assessing a patient with cerebrovascular disease (CVD), a


systematic and thorough approach is essential for accurate diagnosis
and effective management. Here’s a structured method:
• 1. History Taking
• Presenting Symptoms:
• Sudden onset of weakness or numbness (especially unilateral)
• Difficulty speaking or understanding speech
• Vision disturbances (blurred or double vision)
• Dizziness, loss of balance, or coordination issues
• Severe headache (especially in cases of hemorrhage)
• Medical History:
• Previous strokes or transient ischemic attacks (TIAs)
• Risk factors (hypertension, diabetes, hyperlipidemia, smoking, atrial fibrillation)
• Family history of cerebrovascular disease
• Medication History:
• Anticoagulant or antiplatelet therapy
• Other relevant medications
• 2. Physical Examination
• Neurological Examination:
• Assess consciousness and orientation
• Evaluate cranial nerves
• Check motor strength, coordination, and reflexes
• Assess sensory function
• Perform a gait assessment
• Cardiovascular Examination:
• Check blood pressure
• Auscultate for heart murmurs or irregular rhythms
• General Examination:
• Look for signs of other vascular diseases (e.g., peripheral artery disease)
• 3. Diagnostic Imaging
• CT Scan: First-line imaging to rule out hemorrhagic stroke and assess for
ischemic changes.
• MRI: Provides detailed images of brain tissue and may be used if CT findings
are inconclusive.
• Ultrasound: Carotid Doppler studies to assess blood flow in carotid arteries.
• Angiography: May be used to visualize blood vessels and detect blockages or
abnormalities.
• 4. Laboratory Tests
• Complete blood count (CBC)
• Coagulation studies (PT, aPTT)
• Lipid profile
• Blood glucose levels
• Electrolytes and renal function tests
• FAST Acronym for Stroke Awareness
• The FAST acronym is a simple and effective way to help people recognize the signs of
a stroke and emphasize the importance of timely action. Here’s what each letter
stands for:
• F - Facial Weakness:
• Check for drooping on one side of the face. Ask the person to smile and observe if one side is
uneven.
• A - Arm Weakness:
• Ask the person to raise both arms. Look for one arm drifting downward or being unable to lift
as high as the other.
• S - Speech Abnormality:
• Ask the person to repeat a simple sentence. Listen for slurred or strange speech, which can
indicate a problem.
• T - Time to Call Emergency Services:
• If you notice any of these symptoms, call emergency services immediately. Every minute
counts in stroke treatment.
• stroke Syndromes
• Stroke syndromes refer to the specific clinical presentations and
symptoms that result from different types of cerebrovascular
accidents (strokes) based on the areas of the brain affected.
Understanding these syndromes helps in diagnosis and management.
Here are some of the key stroke syndromes:
• 1. Anterior Circulation Syndromes
• Middle Cerebral Artery (MCA) Syndrome:
• Pathophysiology: The MCA supplies a significant portion of the lateral
cerebral cortex, including areas responsible for motor and sensory function.
• Clinical Features:
• Contralateral Hemiparesis: Greater weakness in the arm and face than the leg.
• Contralateral Hemisensory Loss: Similar distribution as motor weakness.
• Aphasia: Expressive (Broca's) or receptive (Wernicke's), depending on the hemisphere.
• Hemineglect: Often seen in right hemisphere strokes affecting attention.
• Visual Field Deficits: Homonymous hemianopia may occur.
• Diagnostic Considerations: CT or MRI to confirm ischemia or hemorrhage.
Transcranial Doppler may assess blood flow.
• Anterior Cerebral Artery (ACA) Syndrome:
• Pathophysiology: The ACA mainly supplies the medial surfaces of the frontal
and parietal lobes.
• Clinical Features:
• Contralateral Leg Weakness and Sensory Loss: More pronounced than in the arm.
• Personality Changes: Impairments in executive function and judgment.
• Cognitive Impairments: Memory and reasoning deficits may occur.
• Urinary Incontinence: Often present due to frontal lobe involvement.
• 2. Posterior Circulation Syndromes
• Vertebrobasilar Stroke:
• Pathophysiology: Affects the vertebral and basilar arteries, supplying the
brainstem, cerebellum, and occipital lobes.
• Clinical Features:
• Dizziness and Ataxia: Common due to cerebellar involvement.
• Bilateral Symptoms: Weakness or sensory loss on both sides of the body.
• Cranial Nerve Signs: Dysphagia, dysarthria, and vertigo.
• Locked-in Syndrome: Quadriplegia with preserved consciousness and vertical eye
movements.
• Posterior Cerebral Artery (PCA) Syndrome:
• Pathophysiology: Supplies the occipital lobe and parts of the temporal lobe,
affecting visual processing.
• Clinical Features:
• Contralateral Homonymous Hemianopia: Loss of the same visual field in both eyes.
• Visual Agnosia: Difficulty recognizing familiar objects despite intact vision.
• Memory Deficits: Particularly if the hippocampus is involved.
• Impulsive Behavior: Can occur with right PCA strokes.
• 3. Lacunar Syndromes
• Lacunar Infarcts:
• Pathophysiology: Result from small vessel disease, often related to chronic
hypertension or diabetes, leading to lipohyalinosis.
• Clinical Features:
• Pure Motor Stroke: Hemiparesis without sensory loss, typically affecting the face and
arm.
• Pure Sensory Stroke: Hemisensory loss without motor involvement.
• Ataxic Hemiparesis: Combination of motor weakness and ataxia.
• Dysarthria-Clumsy Hand Syndrome: Speech difficulties combined with fine motor
deficits.
• 4. Cortical vs. Subcortical Strokes
• Cortical Stroke:
• Features: Presents with complex symptoms like aphasia, agnosia, and neglect.
More likely to have visual field deficits and higher cognitive impairments.
• Imaging: More likely to demonstrate cortical infarctions or hemorrhages on
CT/MRI.
• Subcortical Stroke:
• Features: Simpler motor or sensory deficits without higher cognitive
dysfunction. Often presents with pure motor or sensory syndromes.
• Imaging: Typically shows small, deep infarcts on MRI.
• Anatomy of the Posterior Circulation
• Vertebral Arteries: Supply the cervical spinal cord, brainstem, and
cerebellum.
• Basilar Artery: Formed by the union of the vertebral arteries; supplies the
brainstem, cerebellum, and parts of the occipital lobe.
• Posterior Cerebral Arteries (PCA): Branch from the basilar artery, supplying
the occipital lobe and parts of the temporal lobe.
Imaging Studies for Stroke
Diagnosis
• Imaging studies play a crucial role in the evaluation and management
of stroke patients, helping to determine the type of stroke (ischemic
or hemorrhagic) and guide treatment decisions. Here’s an overview of
the primary imaging modalities used in stroke assessment:
• 1. Computed Tomography (CT) Scan
• Purpose: First-line imaging modality in acute stroke settings.
• Indications:
• Rapid identification of hemorrhagic strokes (e.g., subarachnoid hemorrhage,
intracerebral hemorrhage).
• Detection of early ischemic changes (though less sensitive in the initial hours).
• Advantages:
• Quick and widely available.
• No contraindications for patients with metal implants (e.g., pacemakers).
• Limitations:
• May miss small infarcts or early ischemic signs, particularly in the posterior circulation.
• 2. Magnetic Resonance Imaging (MRI)
• Purpose: Offers a more detailed view of brain tissue and vascular structures.
• Indications:
• Evaluation of ischemic strokes, especially in the posterior circulation.
• Identification of subtle brain lesions and infarcts.
• Assessment of acute and chronic changes.
• Advantages:
• Higher sensitivity for detecting early ischemic changes.
• Can provide additional information on tissue viability (e.g., diffusion-weighted imaging).
• Limitations:
• Longer acquisition time; not always available in emergency settings.
• Contraindications for patients with certain implants or claustrophobia.

• 3. Computed Tomography Angiography (CTA)
• Purpose: Non-invasive imaging of cerebral vessels.
• Indications:
• Evaluation of vascular occlusions, stenosis, or aneurysms.
• Planning for endovascular therapy (e.g., thrombectomy).
• Advantages:
• Rapid acquisition and interpretation.
• Provides a comprehensive view of the cerebral vasculature.
• Limitations:
• Requires contrast material, which may pose risks to patients with renal impairment.
• 4. Magnetic Resonance Angiography (MRA)
• Purpose: Visualization of blood vessels using MRI techniques.
• Indications:
• Similar to CTA for assessing cerebral vascular anatomy.
• Advantages:
• No radiation exposure.
• May be preferable for patients allergic to iodinated contrast.
• Limitations:
• Generally less detailed than CTA for evaluating acute occlusions.
• 5. Transcranial Doppler Ultrasonography (TCD)
• Purpose: Ultrasound technique for assessing blood flow in cerebral arteries.
• Indications:
• Monitoring of cerebral blood flow and detection of emboli.
• Evaluation of vasospasm, particularly after subarachnoid hemorrhage.
• Advantages:
• Non-invasive and portable.
• Can be performed at the bedside.
• Limitations:
• Operator-dependent; may have limited sensitivity for certain conditions.

• Imaging studies are essential for the accurate diagnosis and
management of stroke.
CT and MRI are the cornerstones of initial assessment, while
angiographic techniques help evaluate the vascular anatomy and
inform treatment decisions. Understanding the strengths and
limitations of each modality allows healthcare providers to choose the
most appropriate imaging strategy for each patient. Immediate and
accurate imaging can significantly influence treatment outcomes in
stroke care.
Pathophysiology of Ischemic
Stroke
• Ischemic stroke occurs when blood flow to a part of the brain is
obstructed, resulting in neuronal injury and dysfunction.
Understanding the pathophysiological mechanisms involved is crucial
for effective prevention and treatment. Here’s a detailed overview of
the pathophysiology of ischemic stroke
• 1. Types of Ischemic Stroke
• Thrombotic Stroke: Occurs when a blood clot (thrombus) forms in an artery
supplying blood to the brain, often due to atherosclerosis.
• Embolic Stroke: Occurs when a blood clot or debris forms elsewhere in the body
(commonly the heart) and travels to the brain, blocking a cerebral artery.
• 2. Initiating Events
• Atherosclerosis: The formation of plaques in the arterial walls narrows the
arteries and can lead to thrombus formation.
• Cardiac Sources: Conditions such as atrial fibrillation can lead to the formation of
emboli that travel to the cerebral circulation.
• Other Factors: Hypercoagulable states, vascular dissection, or systemic
hypotension can also contribute to ischemic events.
• 3. Mechanisms of Ischemia
• Reduced Blood Flow: The obstruction of blood vessels leads to decreased perfusion
in the affected brain tissue, resulting in oxygen and nutrient deprivation.
• Cerebral Hemodynamics: The brain relies on a delicate balance of cerebral blood
flow (CBF). A drop in CBF below a critical threshold (approximately 20-25 mL/100
g/min) can lead to cellular injury.
• 4. Cellular and Molecular Responses
• Energy Failure: Neurons depend heavily on aerobic metabolism for ATP production.
Ischemia reduces oxygen and glucose delivery, leading to ATP depletion, which
compromises cellular function.
• Ion Imbalance: Decreased ATP levels disrupt ion pumps (e.g., Na+/K+ ATPase),
resulting in an influx of sodium and calcium ions and efflux of potassium, contributing
to depolarization and cellular swelling.
• 5. Excitotoxicity
• Glutamate Release: Ischemic conditions cause excessive release of glutamate, an
excitatory neurotransmitter. High levels of glutamate overstimulate NMDA
receptors, leading to further calcium influx and neuronal injury.
• Calcium Overload: Increased intracellular calcium activates various enzymes (e.g.,
phospholipases, proteases) that contribute to cellular damage and apoptosis.
• 6. Inflammatory Response
• Microglial Activation: Ischemia activates microglia, the brain's immune cells,
which release pro-inflammatory cytokines and further exacerbate tissue damage.
• Blood-Brain Barrier (BBB) Disruption: Ischemic injury can compromise the
integrity of the BBB, leading to edema and increased infiltration of inflammatory
cells and proteins.
• 7. Apoptosis and Necrosis
• Cell Death Mechanisms: Neuronal injury can lead to both apoptosis
(programmed cell death) and necrosis (uncontrolled cell death), contributing
to the loss of brain tissue and function.
• 8. Penumbra and Core Regions
• Core Area: The central region affected by severe ischemia undergoes rapid
cell death and is referred to as the “core.”
• Penumbra: Surrounding the core is the penumbra, where blood flow is
reduced but not completely occluded. This area is at risk and can potentially
be salvaged with timely intervention.
• 9. Reperfusion Injury
• Restoration of Blood Flow: While restoring blood flow is crucial for recovery, it can
also lead to reperfusion injury due to oxidative stress and inflammation, exacerbating
neuronal injury.
• Conclusion
• The pathophysiology of ischemic stroke is complex and involves multiple
interrelated mechanisms, including reduced blood flow, cellular energy
failure, excitotoxicity, inflammation, and cell death. Understanding these
processes is essential for developing effective therapeutic strategies aimed at
minimizing brain damage and improving outcomes in stroke patients. Timely
intervention is crucial to protect the penumbra and restore function in the
affected brain regions.
Treatment of Acute Ischemic
Stroke
• Overview
• The primary goals in the treatment of Acute Ischemic Stroke (AIS) are
to prevent or reverse brain injury. Key steps include:
• Airway, Breathing, and Circulation (ABCs): Ensure the patient’s vital signs are
stable.
• Blood Sugar Management: Treat hypoglycemia or hyperglycemia based on
finger stick testing.
• Emergency Imaging: Perform a noncontrast head CT to differentiate between
ischemic and hemorrhagic strokes.
• Initial Assessment
• CT Findings: No clinical signs can reliably separate ischemia from
hemorrhage, but:
• Hemorrhage: Often indicated by a more depressed level of consciousness,
high initial blood pressure, or worsening symptoms.
• Ischemia: Symptoms that are maximal at onset or remit suggest ischemia.
• Treatment Categories
• Treatments to minimize tissue infarction and improve outcomes fall
into six categories:
• Medical Support
• IV Thrombolysis
• Endovascular Revascularization
• Antithrombotic Treatment
• Neuroprotection
• Rehabilitation at Stroke Centers
• Medical Support
• Goals
• Optimize cerebral perfusion in the ischemic penumbra.
• Prevent complications from immobility, such as infections and deep vein thrombosis
(DVT).
• Interventions
• Subcutaneous Heparin: Safe for DVT prevention.
• Pneumatic Compression Stockings: Effective for reducing DVT risk.
• Blood Pressure Management:
• Reduce if >220/120 mmHg or if thrombolytic therapy is anticipated (>185/110 mmHg).
• Avoid routine lowering below these thresholds to prevent worsening outcomes.
• Fever Management: Treat with antipyretics and cooling methods.
• Glucose Monitoring: Keep serum glucose between 3.3 mmol/L (60 mg/dL) and 10.0 mmol/L (180
mg/dL).
• Cerebral Edema
• Risk: 5-10% of patients may develop significant edema.
• Management: Water restriction and IV mannitol to raise serum osmolarity;
avoid hypovolemia.
• Hemicraniectomy
• Reduces mortality by 50% in cases of significant edema; recommended for
larger infarcts.
• Intravenous Thrombolysis
• rtPA (Recombinant Tissue Plasminogen Activator)
• Benefits confirmed for IV rtPA within 3 hours of onset.
• Dosage: 0.9 mg/kg (max 90 mg); 10% as a bolus, remainder over 60 minutes.
• Outcomes: Increased rates of minimal disability; small increase in hemorrhage risk.
• Extended Windows: Efficacy confirmed in 3-4.5 hour window in Europe; ongoing studies for
4.5-6 hour window.
• Tenecteplase
• Given as a 0.25 mg/kg IV bolus over 5 seconds.
• Benefits include faster administration and less critical care transport.
• Advanced Imaging
• May help select patients beyond the 4.5-hour window who could benefit from thrombolysis.
Administration of Intravenous Recombinant
Tissue Plasminogen Activator (rtPA) for
Acute Ischemic Stroke (AIS)

• Indications
• The use of rtPA is indicated under the following conditions:
• Clinical Diagnosis: Confirmed acute ischemic stroke.
• Time Frame: Onset of symptoms to time of rtPA administration must be ≤ 4.5
hours.
• Imaging: Non-contrast CT scan shows no hemorrhage or edema exceeding
1/3 of the middle cerebral artery (MCA) territory.
• Age: Patient must be ≥ 18 years old.
• Contraindications
• rtPA should not be administered in the following situations:
• Sustained Hypertension: Blood pressure > 185/110 mmHg despite treatment.
• Bleeding Diathesis: Any condition predisposing to bleeding.
• Recent Head Injury: Any history of head trauma or intracerebral hemorrhage.
• Major Surgery: Surgery within the preceding 14 days.
• Gastrointestinal Bleeding: Occurring within the preceding 21 days.
• Recent Myocardial Infarction: Recent heart attack.
Administration Procedure

1. IV Access: Establish two peripheral IV lines; avoid arterial or central line placement.
2. Eligibility Review: Confirm the patient meets all eligibility criteria for rtPA.
3. Dosage:
1. Administer 0.9 mg/kg IV (maximum dose of 90 mg).
2. Give 10% of the total dose as a bolus, followed by the remainder over 1 hour.
4. Monitoring:
1. Conduct frequent blood pressure monitoring.
2. Ensure no other antithrombotic treatments are administered for 24 hours post-administration.
5. Emergency Protocol:
1. If there is a decline in neurologic status or uncontrolled blood pressure, stop the infusion
immediately.
2. Administer cryoprecipitate and perform emergent brain imaging.
1. .
• Additional Considerations
• Urethral Catheterization: Avoid for ≥ 2 hours post-administration.
Antithrombotic Treatment in
Ischemic Stroke
• latelet Inhibition
• Aspirin is the only antiplatelet agent proven effective for the acute
treatment of ischemic stroke.
• Several antiplatelet agents are effective for secondary prevention of
stroke.

• Key Trials:
• International Stroke Trial (IST)
• Involved 19,435 patients.
• Aspirin dosage: 300 mg/day.
• Results:
• Slightly fewer deaths within 14 days: 9.0% vs 9.4%.
• Significantly fewer recurrent ischemic strokes: 2.8% vs 3.9%.
• No excess of hemorrhagic strokes: 0.9% vs 0.8%.
• Trend toward reduced death or dependence at 6 months: 61.2% vs 63.5%.
• Chinese Acute Stroke Trial (CAST)
• Involved 21,106 patients.
• Aspirin dosage: 160 mg/day.
• Results:
• Small reductions in early mortality: 3.3% vs 3.9%.
• Fewer recurrent ischemic strokes: 1.6% vs 2.1%.
• Reduced dependency at discharge or death: 30.5% vs 31.6%.
• Summary of Aspirin's Efficacy:
• Aspirin is safe and offers a small net benefit in treating acute ischemic
stroke.
• For every 1000 acute strokes treated with aspirin:
• ~9 deaths or nonfatal stroke recurrences prevented in the first few weeks.
• ~13 fewer patients will be dead or dependent at 6 months.
• Combination Therapy: Using aspirin with clopidogrel or ticagrelor
after a minor stroke or TIA is effective in preventing a second stroke.

• Anticoagulation
• Clinical trials show no benefit for routine anticoagulation in primary
treatment of atherothrombotic cerebral ischemia.
• Anticoagulation increases the risk of brain and systemic hemorrhage.
• Conclusion: Routine use of heparin or other anticoagulants is not
warranted for atherothrombotic stroke.
• Exceptions: Anticoagulation may benefit patients with dural sinus
thrombosis to halt progression.
Etiology of Ischemic Stroke

• Overview
• Acute ischemic stroke (AIS) management does not initially depend on
etiology; however, identifying the cause is crucial for recurrence
prevention. Key etiologies include atrial fibrillation and carotid
atherosclerosis, which have established prevention strategies.
• Clinical Evaluation
• A thorough clinical examination is vital for narrowing down potential
stroke causes. Focus areas include:
• Vascular System: Measure blood pressure and assess peripheral circulation.
• Cardiac Assessment: Look for dysrhythmias and murmurs.
• Extremities: Check for peripheral emboli.
• Retinal Examination: Identify effects of hypertension and cholesterol emboli.
• A complete neurologic examination localizes the stroke's anatomical
site. Imaging studies, typically a CT or MRI of the brain, are essential,
especially for thrombolysis candidates.
• Laboratory Testing
• Commonly useful tests include:
• Chest X-ray
• Electrocardiogram (ECG)
• Urinalysis
• Complete Blood Count (CBC)
• Erythrocyte Sedimentation Rate (ESR)
• Metabolic Panel (serum electrolytes, BUN, creatinine, blood glucose)
• Lipid Profile
• Coagulation Studies (PT, PTT)

• Only brain imaging is mandatory before administering IV rtPA; other studies should
not delay treatment.
• Cardioembolic Stroke
• Cardioembolism accounts for about 20% of ischemic strokes,
primarily due to thrombi from heart diseases.
• Common Sources: Nonrheumatic atrial fibrillation, myocardial infarction,
prosthetic valves, and rheumatic heart disease.
• Mechanism: Thrombus formation in the atrium or on heart valves leads to
emboli entering the arterial circulation.
• Symptoms: Sudden onset with maximum deficits at presentation.
• Atrial Fibrillation
• Risk of Stroke: Average annual risk is ~5%.
• CHA2DS2-VASc Score: Used for stroke risk assessment.
• Left Atrial Enlargement: Increases thrombus formation risk.

• Paradoxical Embolization
• Venous thrombi can enter the arterial circulation through a patent
foramen ovale (PFO) or atrial septal defect. Detection methods include:
• Bubble-Contrast Echocardiography: Reveals right-to-left shunts.
• Transcranial Doppler: Monitors for bubble passage into cerebral circulation.
• Bacterial Endocarditis
• Can lead to septic emboli and multifocal cerebral infarcts. Symptoms
suggestive of endocarditis include:
• Multifocal Neurologic Symptoms
• Infarcts of Microscopic Size
• Potential for Large Septic Infarcts
• Artery-to-Artery Embolic Stroke
• Artery-to-artery embolism, primarily from atherosclerotic plaques, is
a significant cause of large-vessel brain ischemia.
• Common Sources: Aortic arch, common carotid artery, internal carotid artery,
vertebral arteries, and basilar arteries.
• Carotid Atherosclerosis
• Location: Commonly affects the common carotid bifurcation and proximal
internal carotid artery.
• Risk Factors: Male gender, older age, smoking, hypertension, diabetes,
hypercholesterolemia.
• Impact: Contributes to approximately 10% of ischemic strokes.
Transient Ischemic Attacks
(TIAs)
• Definition
• Transient Ischemic Attacks (TIAs) are brief episodes of stroke symptoms lasting
less than 24 hours, typically under 1 hour. If imaging reveals a brain infarction,
it's classified as a stroke, regardless of symptom duration. A normal brain scan
does not rule out TIA, as the clinical syndrome itself is diagnostic.
• Causes
• TIAs can result from:
• Emboli to the brain
• In situ thrombosis of an intracranial vessel

• During a TIA, the occluded blood vessel reopens, restoring neurologic function.
• Stroke Risk
• The risk of stroke following a TIA is approximately 10–15% within the
first 3 months, with most events occurring within the first 2 days. The
ABCD2 score can help estimate this risk and guide urgent evaluation
and treatment.

• Treatment
• Urgent Evaluation
• Thrombolysis is contraindicated due to symptom improvement, but
patients may be admitted for rapid intervention if symptoms recur.
• Antiplatelet therapy:
• Combination of aspirin and clopidogrel is more effective than aspirin alone..
• Prevention Strategies
• General Principles
• Effective prevention of stroke involves both medical interventions and lifestyle
modifications. Key strategies include:
1. Control of Modifiable Risk Factors:
1. Particularly hypertension, which should be treated to a target of <130/80 mmHg.
2. The SPRINT trial suggests lowering systolic BP to <120 mmHg can significantly reduce stroke risk.
2. Medications:
1. Statins: Proven to reduce stroke risk, even in patients with normal cholesterol levels. The SPARCL trial
indicated atorvastatin (80 mg/d) benefits secondary stroke prevention.
2. Thiazide diuretics and ACE inhibitors are strongly recommended.
3. Lifestyle Modifications:
1. Smoking cessation is crucial.
• Diabetes management is pivotal for primary and secondary prevention.
• Atherosclerosis Risk Factors
• Key risk factors include:
• Older age
• Diabetes mellitus
• Hypertension
• Tobacco smoking
• Abnormal cholesterol levels
• ABCD2 Score for Stroke Risk
• The ABCD2 score helps assess the 3-month stroke risk post-TIA:


• Interpretation
• Lower Scores (0-3): Indicate low risk for subsequent stroke.
• Higher Scores (4-7): Suggest increasing risk, warranting urgent evaluation and
intervention.

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