- 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
- 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%
</aside>
- 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.