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Transient Ischemic Attack (TIA)

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1. Definition

"A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction."

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2. Pathophysiology

A. Thromboembolism (most common)

• A clot (thrombus or embolus) temporarily occludes a cerebral artery, then spontaneously dissolves before permanent tissue death.
• Sources:
  • Cardiac emboli (atrial fibrillation, valvular disease, intracardiac thrombus)
  • Artery-to-artery emboli (atherosclerotic plaques, especially at the carotid bifurcation)

B. Small Vessel Occlusion (Lacunar TIA)

• Lipohyalinosis or microatheroma occludes small penetrating arteries (lenticulostriate, basilar perforators).
• Strongly associated with hypertension and diabetes.

C. Hemodynamic TIA

• Systemic hypoperfusion (e.g., cardiac failure, severe hypotension) in the setting of pre-existing stenosis.
• Often causes stereotyped, repetitive symptoms triggered by positional changes.

D. Rare Causes

• Hypercoagulable states (antiphospholipid syndrome, thrombophilias)
• Vasculitis (SLE, giant cell arteritis)
• Hematologic disorders (polycythemia vera, sickle cell disease)
• Cervical artery dissection (carotid or vertebral)

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3. Risk Factors

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4. Clinical Features

By Vascular Territory:

Anterior Circulation (Carotid Territory — MCA/ACA)

• Contralateral limb weakness or sensory loss (face, arm, leg)
• Aphasia (dominant hemisphere)
• Amaurosis fugax — transient monocular visual loss ("curtain coming down") from ophthalmic artery ischemia
• Hemineglect (non-dominant hemisphere)

Posterior Circulation (Vertebrobasilar Territory — PCA, PICA, AICA)

• Vertigo, nausea, vomiting
• Diplopia or other cranial nerve palsies
• Dysarthria, dysphagia
• Bilateral or crossed weakness/sensory loss
• Cerebellar ataxia
• Homonymous hemianopia
• "Drop attacks" — sudden loss of postural tone without LOC

Key rule: Isolated vertigo, isolated diplopia, or isolated syncope are generally NOT sufficient for TIA diagnosis unless accompanied by other brainstem/cerebellar signs.

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5. Differential Diagnosis

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6. Diagnostic Workup

Immediate Assessment

Neuroimaging

• DWI (Diffusion-Weighted Imaging) — detects acute ischemia within minutes; reveals small cortical/subcortical infarcts that confirm the event was ischemic.
• CT is insensitive for early ischemic change but useful to rule out hemorrhage if MRI is unavailable.
• FLAIR — shows established infarcts; less sensitive than DWI in the acute phase.

Vascular Imaging

• CT Angiography (CTA) or MR Angiography (MRA) of the head and neck — to evaluate for carotid stenosis, intracranial stenosis, vertebrobasilar disease, dissection.
• Carotid Doppler ultrasound — widely available, evaluates carotid bifurcation.

Cardiac Workup

• Echocardiography (TTE or TEE) — detects intracardiac thrombus, PFO, valvular disease, cardiomyopathy.
• Prolonged cardiac monitoring (Holter/event monitor/implantable loop recorder) — detects paroxysmal atrial fibrillation, especially in cryptogenic TIA.

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7. Risk Stratification: The ABCD² Score

Important caveat: Studies show the ABCD² score has modest discriminatory accuracy when used alone. The AHA/ACC recommends urgent neurovascular workup for ALL TIA patients, regardless of ABCD² score, given the risk that any patient may progress to stroke. (p. 5)

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8. Management

Acute Phase (Emergency Department / Hospital)

Antiplatelet Therapy (non-cardioembolic TIA)

• Dual antiplatelet therapy (DAPT): Aspirin + Clopidogrel for 21 days, then transition to single antiplatelet (aspirin or clopidogrel alone).
  • Evidence: POINT and CHANCE trials showed DAPT significantly reduced stroke risk at 90 days vs. aspirin alone in high-risk TIA/minor stroke.
• Aspirin 160–325 mg loading dose if clopidogrel not available.

Anticoagulation (cardioembolic TIA — e.g., AF)

• Direct oral anticoagulants (DOACs) — apixaban, rivaroxaban, or dabigatran preferred over warfarin for non-valvular AF.
• Warfarin — for valvular AF or mechanical heart valves.
• Timing depends on infarct size and bleeding risk.

Blood Pressure Management

• Do not aggressively lower BP acutely in the first 24–48 hours unless hypertensive emergency.
• Long-term target: < 130/80 mmHg (AHA 2019 guidelines).

Statin Therapy

• High-intensity statin (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) started immediately regardless of baseline LDL.
• Evidence: SPARCL trial showed atorvastatin 80 mg reduced recurrent stroke/TIA.

Surgical/Interventional Management

Secondary Prevention (Long-term)

• Antiplatelet or anticoagulation (depending on mechanism)
• Aggressive BP control
• Statin therapy
• Glycemic control in diabetics
• Smoking cessation
• Weight loss, exercise, dietary modification
• Closure of PFO in selected patients (< 60 years, cryptogenic TIA/stroke, large shunt on echo)

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9. Prognosis

• Short-term stroke risk is highest in the first 48 hours:
  • ~3–10% risk of stroke within 2 days
  • ~9–17% risk within 90 days
• TIA is a strong predictor of future stroke — it is sometimes called a "warning stroke."
• With rapid, aggressive management (urgent workup + secondary prevention), the 90-day stroke risk can be reduced by up to 80% (EXPRESS and SOS-TIA studies).
• Patients with DWI-positive TIA (i.e., small infarct on MRI) have a higher risk of early recurrent stroke than DWI-negative TIA.

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10. Special Populations

Pediatric TIA

• Rare; causes differ — sickle cell disease, congenital heart disease, prothrombotic states, moyamoya disease.
• Workup is broader (including metabolic and genetic studies).

Pregnancy

• Increased risk due to hypercoagulable state, peripartum cardiomyopathy, eclampsia.
• MRI preferred (no radiation); anticoagulation with LMWH if needed (DOACs are contraindicated).

Elderly (> 80 years)

• Higher risk of AF as underlying etiology.
• Risk-benefit analysis of anticoagulation must account for fall risk and bleeding tendency.

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Summary Table

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