TIA (Transient Ischaemic Attack) - Adult

Quick Reference

Critical Alerts

⚠️ Red Flag: - TIA is a medical emergency - 10-15% risk of stroke within 90 days, with highest risk in first 48-72 hours [1,2]

• Tissue-based definition now standard - absence of infarction on DWI-MRI, not symptom duration [3]
• 30-40% of clinical "TIAs" show DWI lesions - these represent minor strokes with infarction [4]
• Start dual antiplatelet immediately - aspirin + clopidogrel loading reduces stroke by 30% [5,6]
• Urgent carotid imaging essential - CEA within 2 weeks for symptomatic ≥70% stenosis [7]
• EXPRESS study showed 80% risk reduction with urgent treatment vs standard care [8]

Key Diagnostics

Emergency Treatments

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Definition and Modern Concepts

Evolving Definition of TIA

The understanding of transient ischaemic attack has undergone a paradigm shift from a time-based to a tissue-based definition, fundamentally changing clinical approach and risk stratification. [3]

Classical Time-Based Definition (Historical) Transient episode of neurological dysfunction lasting less than 24 hours, presumed to be caused by focal brain, spinal cord, or retinal ischaemia.

Modern Tissue-Based Definition (Current Standard) Transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction on neuroimaging. [3]

Exam Detail: Why the Definition Changed

The 2009 AHA/ASA scientific statement redefined TIA based on several key observations: [3]

1. Arbitrary 24-hour threshold: The 24-hour cutoff was arbitrary with no biological basis - most TIAs resolve within 60 minutes
2. DWI-MRI sensitivity: 30-50% of patients with symptoms lasting less than 24 hours have evidence of infarction on DWI-MRI [4]
3. Prognostic implications: Presence of DWI lesion indicates completed infarction regardless of symptom duration
4. Treatment implications: Tissue injury defines stroke, not symptom duration

Clinical Implications of Tissue-Based Definition:

• MRI with DWI is the gold standard for distinguishing TIA from minor stroke
• "TIA" with positive DWI = minor ischaemic stroke (tissue injury present)
• "TIA" with negative DWI = true TIA (no tissue injury)
• Both require urgent evaluation and treatment

Terminology Clarification

Why TIA Matters: The Warning Stroke

TIA represents a critical window of opportunity for stroke prevention. The concept of "brain attack" emphasises the urgency comparable to myocardial infarction. [1,2]

Short-Term Stroke Risk After TIA:

The EXPRESS study (2007) demonstrated that urgent TIA clinic evaluation with immediate treatment initiation reduced 90-day stroke risk by 80% compared to standard care (10.3% vs 2.1%, p=0.0001). [8]

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Epidemiology

Incidence and Prevalence

TIA incidence varies by population, diagnostic criteria, and healthcare access. The shift to tissue-based definitions has refined epidemiological understanding. [11]

Demographics

Age Distribution:

• Median age at TIA: 72 years
• Incidence doubles every decade after age 55
• Rare before age 45 (consider alternative diagnoses)

Sex Differences:

• Men: Higher incidence before age 75
• Women: Higher incidence after age 75
• Similar overall lifetime risk

Ethnic Variations:

• African Americans: 38% higher risk than Caucasians
• Hispanic populations: Intermediate risk
• Asian populations: Higher proportion of intracranial disease

Temporal Patterns

• Peak incidence: 8:00-11:00 AM (morning surge)
• Seasonal variation: Higher in winter months
• Circadian rhythm correlates with blood pressure and platelet activation

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Pathophysiology

Mechanism of Transient Ischaemia

TIA results from temporary interruption of cerebral blood flow insufficient to cause permanent tissue injury. The pathophysiological mechanisms mirror those of ischaemic stroke. [3]

Transient Vascular Occlusion (embolic or thrombotic)
                ↓
    Focal Cerebral Hypoperfusion
                ↓
    Ischaemic Penumbra Development
                ↓
    Neurological Symptoms Manifest
                ↓
    Spontaneous Reperfusion/Collateral Recruitment
                ↓
    Symptoms Resolve (No Infarction)

Exam Detail: Ischaemic Cascade (Molecular Level)

The transient nature of TIA involves incomplete activation of the ischaemic cascade:

1. Energy failure (seconds): ATP depletion, ionic pump failure
2. Glutamate excitotoxicity (minutes): NMDA receptor activation
3. Calcium influx: Intracellular Ca²⁺ accumulation
4. Oxidative stress: Reactive oxygen species generation
5. Mitochondrial dysfunction: Cytochrome c release

Why No Permanent Injury?

• Rapid reperfusion (less than 60 minutes typically)
• Collateral circulation activation
• Ischaemic penumbra salvaged
• Incomplete cascade activation
• Ischaemic preconditioning in some patients

Penumbra Concept: The ischaemic penumbra represents tissue at risk surrounding the ischaemic core. In TIA, the entire affected territory functions as salvaged penumbra due to timely reperfusion.

Aetiological Classification (TOAST/Oxford)

Understanding the underlying mechanism guides secondary prevention strategy. [12]

Exam Detail: Large Artery Atherosclerosis - Mechanism Details

Carotid stenosis causes TIA through three main mechanisms:

1. Artery-to-artery embolism (most common)

   • Unstable plaque with thrombus formation
   • Platelet-fibrin emboli to distal vessels
   • Often ulcerated or irregular plaque

2. Haemodynamic compromise

   • Critical stenosis (> 90%) with flow limitation
   • Watershed territory symptoms
   • Postural symptoms possible

3. In-situ thrombosis

   • Acute plaque rupture with thrombotic occlusion
   • Transient before spontaneous lysis

Cardioembolic Sources (High-Risk):

• Atrial fibrillation (accounts for 50% of cardioembolic strokes)
• Left ventricular thrombus
• Mechanical heart valves
• Infective endocarditis
• Left atrial appendage thrombus
• Dilated cardiomyopathy (EF less than 35%)

Cardioembolic Sources (Medium-Risk):

• Patent foramen ovale (controversial)
• Atrial septal aneurysm
• Aortic arch atheroma (> 4 mm)
• Mitral valve prolapse
• Mitral annular calcification

Risk Factors

Population Attributable Risk (Key Statistics): [13]

• Hypertension: 35% of stroke risk attributable
• Smoking: 19% of stroke risk attributable
• Obesity: 19% of stroke risk attributable
• Physical inactivity: 36% of stroke risk attributable
• Diet: 23% of stroke risk attributable

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Clinical Presentation

Symptom Patterns by Vascular Territory

Clinical presentation depends on the arterial territory affected. Recognition of vascular patterns aids diagnosis and guides imaging.

Anterior Circulation (Carotid Territory)

Posterior Circulation (Vertebrobasilar Territory)

Clinical Pearl: Isolated Vertigo - Is It TIA?

Isolated vertigo is rarely due to posterior circulation TIA. Suspect TIA only when vertigo is accompanied by other posterior circulation symptoms:

• Diplopia
• Dysarthria
• Dysphagia
• Ataxia
• Crossed sensory/motor findings

Use the HINTS exam to differentiate peripheral from central vertigo:

• Head Impulse test (normal = central)
• Nystagmus type (direction-changing = central)
• Test of Skew (skew deviation = central)

A benign HINTS pattern has higher sensitivity for ruling out stroke than early MRI (98% vs 80%).

Duration and Timing

Key Point: Most true TIAs last 10-15 minutes. Symptoms lasting > 1 hour significantly increase probability of DWI lesion (infarction). [4]

TIA Mimics (Differential Diagnosis)

Up to 60% of patients referred with suspected TIA have alternative diagnoses. [14]

Physical Examination

Often Normal by Presentation

The examination is frequently unremarkable as symptoms have resolved. However, examine for:

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Red Flags and High-Risk Features

Immediate High-Risk Indicators

⚠️ Red Flag: | Red Flag | Clinical Concern | Immediate Action | |----------|-----------------|------------------| | Ongoing symptoms | Active stroke | Stroke protocol, consider thrombolysis | | Crescendo TIAs (≥2 in 24h) | Unstable plaque, imminent stroke | Admission, expedited carotid imaging | | ABCD2 score ≥4 | 4% 48-hour stroke risk | Consider admission | | Known carotid stenosis ≥50% | Symptomatic stenosis, treatable | Urgent surgery evaluation | | Atrial fibrillation | Cardioembolic source | Anticoagulation | | Recent carotid intervention | Restenosis, hyperperfusion | Urgent imaging | | Amaurosis fugax + carotid bruit | High-grade carotid disease | Urgent CEA evaluation | | DWI lesion on MRI | Minor stroke (not TIA) | Higher recurrence risk | | Large artery stenosis/occlusion | Haemodynamic or embolic | Consider intervention |

Crescendo TIA - A Stroke Emergency

Crescendo TIA describes multiple TIAs occurring over hours to days, indicating:

• Unstable atherosclerotic plaque
• Critical stenosis with flow limitation
• High-risk cardioembolic source
• Imminent stroke

Management:

• Hospital admission mandatory
• Continuous telemetry monitoring
• Expedited carotid imaging (same day)
• Consider dual antiplatelet therapy
• Early surgical consultation if carotid disease
• BP permissive (avoid hypotension)

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Risk Stratification

ABCD2 Score

The ABCD2 score stratifies short-term stroke risk after TIA. Despite limitations, it remains widely used for disposition decisions. [15]

Risk Stratification by ABCD2 Score:

Exam Detail: Limitations of ABCD2 Score

The ABCD2 score has significant limitations that should be recognised: [15]

1. Does not include imaging findings - DWI lesion and carotid stenosis independently predict stroke
2. Lower scores do not exclude high-risk aetiology - AF or critical stenosis may have ABCD2 = 2
3. Variable performance - Validation studies show AUC 0.62-0.72
4. Does not differentiate TIA mimics - May "score" non-vascular causes

Enhanced Risk Scores:

ABCD2-I (adds imaging):

• Add 2 points for DWI lesion
• Add 2 points for carotid stenosis ≥50%

ABCD3-I (adds dual TIA):

• Add 2 points for dual TIA (≥2 in 7 days)
• Add 2 points for DWI lesion
• Add 2 points for ≥50% stenosis

These modified scores improve discrimination (AUC 0.74-0.82) but are less widely implemented.

Clinical Decision Rules for Disposition

Consider Admission If:

• ABCD2 score ≥4
• Crescendo TIAs
• Symptomatic carotid stenosis ≥50%
• Known or newly detected atrial fibrillation
• Positive DWI on MRI
• Unable to complete urgent outpatient workup within 24-48 hours
• Residual neurological deficit
• Unreliable patient or poor social circumstances
• Unable to return rapidly if symptoms recur

Outpatient TIA Clinic Appropriate If:

• ABCD2 score 0-3
• No high-risk features above
• Brain imaging and carotid imaging completed or arranged within 24 hours
• Antiplatelet therapy initiated
• Reliable patient with ability to return
• Close follow-up arranged (within 24-48 hours)

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Diagnostic Approach

Structured Investigation Algorithm

Phase 1: Immediate (Emergency Department)

Phase 2: Urgent (Within 24 Hours)

Phase 3: Extended (Within 7-14 Days)

Neuroimaging

CT Head

• First-line to exclude haemorrhage
• Low sensitivity for acute ischaemia (10-20%)
• May show old infarcts, tumours, other pathology
• Cannot distinguish TIA from minor stroke

MRI Brain with DWI (Gold Standard) [4]

• Detects acute ischaemia within minutes of onset
• Sensitivity 80-90% for acute infarction
• 30-50% of "clinical TIAs" have DWI lesion (= minor stroke)
• Informs prognosis: DWI+ patients have 3-4x higher recurrence risk
• Should be performed within 24 hours when possible

Clinical Pearl: DWI-MRI Interpretation Pearls

• DWI bright + ADC dark = acute ischaemia (cytotoxic oedema)
• DWI bright + ADC bright = T2 shine-through (not acute)
• Small DWI lesions may not have corresponding ADC change
• Posterior fossa lesions harder to detect (susceptibility artifact)
• False negatives occur in first 6 hours and for very small lesions
• Serial MRI can detect new lesions indicating ongoing embolism

Carotid Imaging

Carotid stenosis is the most treatable cause of TIA. All patients require carotid assessment.

NASCET vs ECST Measurement Methods:

• NASCET: Stenosis relative to normal distal ICA (most commonly used)
• ECST: Stenosis relative to estimated original lumen
• Conversion: ECST 70% ≈ NASCET 50%; ECST 85% ≈ NASCET 70%

Cardiac Evaluation

ECG Findings:

Echocardiography Indications:

• All TIA patients (TTE as minimum)
• TEE if: suspected cardioembolic, young patient, cryptogenic TIA, PFO evaluation
• Bubble study (agitated saline contrast) for PFO detection

Extended Cardiac Monitoring for Occult AF: [16]

The CRYSTAL-AF trial demonstrated that implantable cardiac monitors detected AF in 30% of cryptogenic stroke/TIA patients over 3 years, compared to 3% with standard monitoring. [16]

Laboratory Investigations

Extended Investigations (Selected Patients):

• Thrombophilia screen: Young, unprovoked, family history
• Vasculitis screen: Systemic symptoms, young patient
• Lumbar puncture: Suspected CNS vasculitis, infection
• Toxicology: Young patient, cocaine/amphetamine use

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Treatment

Immediate Antiplatelet Therapy

Antiplatelet therapy is the cornerstone of TIA management and should be initiated immediately in the emergency department unless contraindicated. [5,6]

Single Antiplatelet Therapy (All TIA Patients)

Dual Antiplatelet Therapy (DAPT) - High-Risk TIA [5,6]

The CHANCE and POINT trials established dual antiplatelet therapy as standard for high-risk TIA:

Exam Detail: CHANCE Trial (Clopidogrel in High-Risk Patients with Acute Non-disabling Cerebrovascular Events) [6]

• Population: 5,170 Chinese patients with TIA (ABCD2 ≥4) or minor stroke (NIHSS ≤3)
• Intervention: Aspirin 75 mg + Clopidogrel 75 mg (after 300 mg load) vs Aspirin 75 mg alone
• Duration: 21 days of DAPT
• Primary Outcome: Stroke at 90 days: 8.2% vs 11.7% (HR 0.68, pless than 0.001)
• Bleeding: No significant difference in major haemorrhage
• Conclusion: Short-term DAPT superior to aspirin alone in Chinese population

POINT Trial (Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke) [5]

• Population: 4,881 international patients with TIA (ABCD2 ≥4) or minor stroke (NIHSS ≤3)
• Intervention: Aspirin 50-325 mg + Clopidogrel 600 mg load then 75 mg vs Aspirin alone
• Duration: 90 days of DAPT
• Primary Outcome: Major ischaemic events: 5.0% vs 6.5% (HR 0.75, p=0.02)
• Bleeding: Major haemorrhage: 0.9% vs 0.4% (HR 2.32, p=0.02)
• Conclusion: Benefit primarily in first 21 days; bleeding risk increases with duration

Synthesis - Current Practice:

• DAPT for 21 days is optimal balance of efficacy and safety
• Start within 12-24 hours of symptom onset
• After 21 days, continue single antiplatelet (aspirin or clopidogrel)
• DAPT reduces stroke by ~30% but increases major bleeding modestly

Current DAPT Recommendations:

Contraindications to Antiplatelet Therapy:

• Active significant bleeding
• Severe thrombocytopenia
• Known hypersensitivity
• Planned urgent surgery
• Anticoagulation indication (AF - switch to anticoagulant)

Statin Therapy

High-intensity statin therapy is recommended for all patients with TIA of presumed atherosclerotic origin. [9]

SPARCL Trial (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) [9]

• Atorvastatin 80 mg vs placebo in stroke/TIA patients
• 16% reduction in recurrent stroke (HR 0.84)
• 35% reduction in major cardiovascular events
• Benefit independent of baseline LDL

Targets:

• LDL cholesterol: less than 1.8 mmol/L (70 mg/dL) for very high-risk

• 50% reduction from baseline if target not achievable

• Consider PCSK9 inhibitors if target not achieved on maximum statin

Blood Pressure Management

Hypertension is the most important modifiable risk factor for stroke. Management differs in acute versus chronic phases. [10]

Acute Phase (First 24-48 Hours):

• Permissive hypertension (avoid lowering unless extreme)
• Do not treat unless BP > 220/120 mmHg
• Rationale: Maintain cerebral perfusion through collaterals
• Exception: If thrombolysis candidate (different thresholds apply)

Chronic Secondary Prevention:

Current Targets: [10]

• General target: less than 130/80 mmHg
• Severe bilateral carotid stenosis: More liberal (individual assessment)
• Elderly (> 80 years): less than 140/90 mmHg may be acceptable

Preferred Agents:

• ACE inhibitors (perindopril has best evidence)
• Thiazide diuretics (indapamide)
• Calcium channel blockers
• Combination therapy usually required

Carotid Revascularisation

Carotid endarterectomy (CEA) is highly effective for preventing stroke in symptomatic carotid stenosis. Timing and patient selection are critical. [7,17]

Indications for Carotid Endarterectomy:

Exam Detail: Landmark Carotid Surgery Trials

NASCET (North American Symptomatic Carotid Endarterectomy Trial) [7]

• 2,226 patients with symptomatic carotid stenosis
• For 70-99% stenosis: 2-year ipsilateral stroke risk 9% vs 26% (CEA vs medical)
• Absolute risk reduction: 17% (NNT = 6)
• For 50-69% stenosis: Modest benefit (ARR 6.5% at 5 years)

ECST (European Carotid Surgery Trial) [17]

• Similar findings to NASCET
• Confirmed benefit for severe stenosis
• Different measurement methodology

Key Surgical Principles:

• Timing: Operate within 2 weeks of TIA (greatest benefit)
• Delay reduces benefit: 14% reduction in benefit per week of delay
• Surgical risk: less than 6% perioperative stroke/death rate required for net benefit
• No benefit for less than 50% stenosis: Medical therapy alone

Carotid Artery Stenting (CAS) vs CEA:

The CREST trial showed equivalent long-term outcomes for CEA and CAS, but differing short-term risk profiles:

• CEA: Higher MI risk (2.3% vs 1.1%)
• CAS: Higher stroke risk (4.1% vs 2.3%)

Contraindications to Carotid Surgery:

• Chronic total occlusion
• Severe disability from prior stroke
• Limited life expectancy
• High surgical risk with low-grade stenosis

Anticoagulation for Atrial Fibrillation

If atrial fibrillation is detected, anticoagulation replaces antiplatelet therapy for secondary prevention. [18]

Timing of Anticoagulation After TIA:

• TIA with no infarction on imaging: Start immediately (1-3 days)
• Minor stroke (small infarct): Start at 3-5 days
• Moderate stroke: Start at 5-7 days
• Large stroke: Start at 7-14 days (haemorrhagic transformation risk)

CHA₂DS₂-VASc Score:

• Score ≥2 (male) or ≥3 (female): Anticoagulation recommended
• TIA/stroke adds 2 points → virtually all TIA patients with AF require anticoagulation

Anticoagulant Options: [18]

DOACs vs Warfarin Post-Stroke/TIA:

• DOACs have lower intracranial bleeding risk
• Similar or better efficacy for stroke prevention
• No routine monitoring required
• Preferred for non-valvular AF

Lifestyle Modifications

Comprehensive lifestyle intervention is essential for secondary prevention.

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Disposition and Follow-Up

Emergency Department Disposition

Admission Criteria:

• ABCD2 score ≥4 and unable to complete urgent outpatient workup
• Crescendo TIAs
• Symptomatic carotid stenosis ≥50% confirmed
• Newly detected atrial fibrillation requiring anticoagulation initiation
• Positive DWI on MRI (minor stroke)
• Residual neurological deficit
• Unable to obtain timely outpatient imaging
• Unreliable patient or poor social circumstances
• Patient unable to return quickly if symptoms recur

Discharge with Urgent Outpatient Follow-Up:

• Low-risk TIA (ABCD2 0-3) with no high-risk features
• Brain imaging completed or arranged within 24 hours
• Carotid imaging completed or arranged within 24 hours
• Antiplatelet therapy initiated
• Statin therapy initiated
• Reliable patient with ability to return
• Clear return precautions provided
• Follow-up arranged within 24-48 hours

Discharge Checklist

Follow-Up Schedule

Driving Regulations (UK DVLA)

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Special Populations

Young Adults (less than 45 Years)

Unusual causes are more prevalent in young patients:

Investigation Approach:

• Standard TIA workup PLUS:
• MRA/CTA including vessel wall imaging
• TEE with bubble study (PFO evaluation)
• Thrombophilia screen
• Vasculitis screen if indicated
• Consider lumbar puncture if CNS vasculitis suspected

Elderly (> 80 Years)

Pregnancy

TIA in pregnancy requires specialist multidisciplinary management:

Cryptogenic TIA

When standard workup is negative, extended evaluation may reveal occult causes:

ESUS (Embolic Stroke of Undetermined Source) Approach:

• Prolonged cardiac monitoring (≥30 days)
• TEE for aortic arch atheroma and PFO
• Consider implantable loop recorder
• PFO closure in selected patients (less than 60 years, high-risk PFO features)

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Prognosis

Short-Term Outcomes

Long-Term Outcomes

Prognostic Factors

Poor Prognosis:

• High ABCD2 score
• DWI lesion on MRI
• Carotid stenosis ≥50%
• Atrial fibrillation
• Multiple TIAs
• Diabetes mellitus
• Persistent risk factors

Good Prognosis:

• Single brief TIA
• Prompt treatment initiation
• Negative DWI-MRI
• No carotid disease
• Excellent risk factor control
• High adherence to medications

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Patient Education

Understanding TIA

Key messages for patients:

• TIA is a "warning stroke"
• brain ischaemia without permanent damage
• The risk of a complete stroke is highest in the next few days
• Urgent treatment and evaluation significantly reduces stroke risk
• Medication adherence and lifestyle changes are essential
• Know the signs of stroke and call emergency services immediately

FAST Stroke Recognition

Medication Adherence

Lifestyle Modification Counselling

Return Precautions

Return to Emergency Department Immediately If:

• Any new weakness, numbness, or paralysis
• New speech difficulty (slurred or confused)
• New vision changes
• Severe sudden headache
• Symptoms similar to your TIA that return
• Any symptoms lasting more than a few minutes

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Viva Preparation

Common Viva Questions

Viva Point: Q: A 68-year-old man presents with resolved right arm weakness lasting 20 minutes. How would you approach this?

Opening Statement: "This presentation is concerning for a transient ischaemic attack, which represents a medical emergency given the high short-term stroke risk. My approach would be systematic, focusing on confirming the diagnosis, risk stratifying, initiating immediate treatment, and arranging urgent investigation."

Structured Answer:

1. Immediate assessment: ABC, glucose, full neurological examination
2. Confirm TIA: Symptoms consistent with vascular territory, resolved completely
3. Risk stratify: Calculate ABCD2 score (age ≥60 = 1, BP ≥140/90 = 1, unilateral weakness = 2, duration 10-59 min = 1, diabetes = check) = likely 4-5 (moderate-high risk)
4. Immediate treatment: Aspirin 300 mg stat, consider dual antiplatelet if ABCD2 ≥4
5. Investigations: CT head, ECG, bloods (glucose, lipids, HbA1c), arrange urgent MRI and carotid imaging
6. Disposition: Consider admission given high-risk score; alternatively, urgent TIA clinic within 24 hours if imaging arranged

Viva Point: Q: What is the evidence for dual antiplatelet therapy in TIA?

Key Evidence: "Two landmark trials established dual antiplatelet therapy for high-risk TIA:

1. CHANCE trial (2013): Chinese population, aspirin plus clopidogrel for 21 days reduced 90-day stroke from 11.7% to 8.2% (32% relative risk reduction) with no increase in major bleeding.

2. POINT trial (2018): International population, aspirin plus clopidogrel for 90 days reduced major ischaemic events from 6.5% to 5.0% (25% RRR) but with increased major bleeding (0.9% vs 0.4%).

The synthesis is that 21 days of DAPT provides optimal balance - most stroke prevention benefit occurs early, while bleeding risk increases with prolonged therapy. Current guidelines recommend DAPT for 21 days in high-risk TIA (ABCD2 ≥4) or minor stroke, followed by single antiplatelet therapy."

Viva Point: Q: When would you refer for carotid endarterectomy?

Answer: "Carotid endarterectomy is indicated for symptomatic carotid stenosis ≥70% (NASCET criteria) and should be performed within 2 weeks of the index event.

Key points from NASCET:

• 70-99% stenosis: 2-year stroke risk 9% with CEA vs 26% medical therapy (NNT = 6)
• 50-69% stenosis: Modest benefit (NNT = 22), decision individualised
• less than 50% stenosis: No benefit from surgery

Timing is critical: Benefit decreases by 14% for each week of delay. Surgery should be performed within 2 weeks, ideally within first week.

Patient selection: Perioperative stroke/death rate must be less than 6% for net benefit. CAS is alternative for high surgical risk or anatomically unfavourable cases."

Model Answers for Common Scenarios

Scenario 1: TIA with 80% carotid stenosis

"This patient has symptomatic severe carotid stenosis and requires urgent carotid endarterectomy within 2 weeks. Immediate management includes dual antiplatelet therapy, high-intensity statin, and blood pressure optimisation. Surgical referral should occur within 24-48 hours with target intervention within 2 weeks."

Scenario 2: TIA with new atrial fibrillation

"This is a cardioembolic TIA. Anticoagulation is indicated and will replace long-term antiplatelet therapy. Given no infarction on imaging, I would initiate a DOAC within 1-3 days. Apixaban is preferred given its favourable bleeding profile. CHA₂DS₂-VASc score is at least 2 (stroke = 2 points), confirming anticoagulation indication."

Scenario 3: Young patient (35 years) with TIA

"In young patients, I would consider unusual causes including arterial dissection, PFO with paradoxical embolism, vasculitis, and hypercoagulable states. Investigation would include MRA neck with vessel wall imaging, TEE with bubble study, thrombophilia screen, and vasculitis markers. Standard secondary prevention applies pending results."

Common Mistakes (What Fails Candidates)

⚠️ Red Flag: Avoid These Errors:

❌ Failing to recognise TIA as a medical emergency ❌ Not initiating antiplatelet therapy immediately ❌ Using outdated 24-hour time-based definition ❌ Not arranging urgent carotid imaging for all patients ❌ Forgetting to check for atrial fibrillation ❌ Not knowing DAPT duration (21 days, not 90 days) ❌ Wrong NASCET stenosis thresholds for CEA (≥70% = strong, 50-69% = moderate) ❌ Failing to counsel on driving restrictions ❌ Not knowing landmark trials (CHANCE, POINT, NASCET, SPARCL) ❌ Missing the distinction between TIA (no infarct) and minor stroke (DWI+)

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Key Guidelines

International Guidelines Summary

Evidence Strength Summary

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Clinical Pearls Summary

Clinical Pearl: Diagnostic Pearls:

1. TIA is a clinical diagnosis - symptoms resolved, investigations may be negative
2. 30-50% of "clinical TIAs" are actually minor strokes (DWI positive)
3. ABCD2 score underestimates risk - add imaging and carotid findings
4. Amaurosis fugax strongly suggests carotid source
5. Isolated vertigo is rarely TIA - require additional posterior circulation symptoms
6. AF may be paroxysmal - extended monitoring detects 25-30% occult AF

Treatment Pearls:

1. Start aspirin immediately - don't wait for imaging (unless haemorrhage suspected)
2. DAPT for 21 days in high-risk TIA - not 90 days (bleeding risk increases)
3. Carotid surgery within 2 weeks - benefit decreases by 14% per week delay
4. High-intensity statin for all (SPARCL trial)
5. BP control chronic phase only - permissive acutely
6. DOACs preferred over warfarin for AF-related TIA

Disposition Pearls:

1. Low-risk TIA can be managed outpatient IF urgent workup ensured
2. High-risk (ABCD2 ≥4, carotid disease, AF) - consider admission
3. Crescendo TIAs warrant admission - unstable condition
4. Close follow-up essential - highest stroke risk first 48 hours
5. Ensure patient understands FAST signs and when to return

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References

1. Amarenco P, Lavallée PC, Labreuche J, et al. One-year risk of stroke after transient ischemic attack or minor stroke. N Engl J Med. 2016;374(16):1533-1542. doi:10.1056/NEJMoa1412981

2. Coull AJ, Lovett JK, Rothwell PM; Oxford Vascular Study. Population based study of early risk of stroke after transient ischaemic attack or minor stroke: implications for public education and organisation of services. BMJ. 2004;328(7435):326. doi:10.1136/bmj.37991.635266.44

3. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2009;40(6):2276-2293. doi:10.1161/STROKEAHA.108.192218

4. Coutts SB, Simon JE, Eliasziw M, et al. Triaging transient ischemic attack and minor stroke patients using acute magnetic resonance imaging. Ann Neurol. 2005;57(6):848-854. doi:10.1002/ana.20497

5. Johnston SC, Easton JD, Farrant M, et al. Clopidogrel and aspirin in acute ischemic stroke and high-risk TIA. N Engl J Med. 2018;379(3):215-225. doi:10.1056/NEJMoa1800410

6. Wang Y, Wang Y, Zhao X, et al. Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Engl J Med. 2013;369(1):11-19. doi:10.1056/NEJMoa1215340

7. Barnett HJM, Taylor DW, Haynes RB, et al. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325(7):445-453. doi:10.1056/NEJM199108153250701

8. Rothwell PM, Giles MF, Chandratheva A, et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. 2007;370(9596):1432-1442. doi:10.1016/S0140-6736(07)61448-2

9. Amarenco P, Bogousslavsky J, Callahan A III, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006;355(6):549-559. doi:10.1056/NEJMoa061894

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