• TIA refers to temporary, focal cerebral ischemia that results in reversible neurological deficits without acute infarction (i.e., imaging findings show no signs of infarction).
• Cardiogenic embolism and atherosclerosis are the most commonly identified mechanisms of TIAs, although an underlying etiology is not always identified.

Neurological manifestations

• Acute, transient focal neurological symptoms

• Typically, symptoms last < 1 hour (the majority of cases resolve in < 15 minutes).

• Possibly amaurosis fugax

  Amaurosis fugax

• Symptoms depend on the affected territory

Features suggesting a specific underlying cause

• Atrial fibrillation: palpitations, irregular heart rate
• Carotid artery stenosis: carotid bruit
• Endocarditis: fever, heart murmur, history of IV drug abuse
• Aortic dissection: chest pain, hypotension
• Paradoxical embolism (PFO): features of DVT

<aside> 📈 Increased risk of future ischemic stroke! Within 2 days: ∼ 3–10% → Within 90 days: ∼ 9–17%

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• Patients with TIA are at markedly increased risk of future stroke; therefore, intensive medical management is indicated.  Secondary prevention includes:
  • antiplatelet agents (eg, aspirin, clopidogrel) to prevent thrombus formation
  • statin therapy (HMG-CoA reductase inhibitor; eg, atorvastatin, rosuvastatin) to reduce atherosclerotic plaque formation
  • Lifestyle modifications (eg, exercise, tobacco cessation)

In addition to optimal blood pressure control and statin therapy, low-dose aspirin is commonly used to prevent ischemic stroke in patients with TIA.  It works by irreversibly acetylating/inhibiting the cyclooxygenase (COX) enzymes.  At low doses, aspirin predominantly inhibits COX-1, preventing platelet synthesis of thromboxane A2, which impairs platelet aggregation and reduces vasoconstriction.

At least 2 distinct COX-1-dependent mechanisms contribute to the increased risk of upper gastrointestinal (GI) bleeding associated with aspirin therapy: Inhibition of platelet aggregation and impairment of prostaglandin-dependent GI mucosal protection.  The risk of upper GI bleeding increases with higher doses but is increased 2- to 3-fold even with low-dose aspirin.  Proton pump inhibitors can help reduce the risk of upper GI bleeding in patients taking aspirin.