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Transient Ischemic Attacks
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by focal cerebral ischemia without acute infarction. TIAs are often called "ministrokes" or "warning strokes" as they confer a high short-term risk of subsequent ischemic stroke, with 10-20% of patients suffering a stroke within 90 days. Around 50% of strokes occur within 48 hours after a TIA.
Pathophysiology:
TIAs arise from a transient disruption of blood flow to a region of the brain, most commonly due to emboli or local thrombosis from atherosclerotic plaque rupture. Less frequent causes include vasospasm, venous thrombosis, or hemodynamic factors like artery dissection or severe stenosis. The topography of symptoms reflects the vascular territory affected.
Clinical Presentation:
TIA symptoms are negative (loss of function) rather than positive phenomena like headaches or visual auras seen in migraines. Typical TIA symptoms include unilateral motor weakness, dysarthria, monocular blindness, or sensory deficits corresponding to the area of transiently disrupted blood flow. By definition, symptoms completely resolve within 24 hours.
Diagnostic Workup:
The diagnostic workup aims to determine the underlying etiology, assess future stroke risk, and guide preventative therapy. Essentials include brain imaging such as CT or MRI, neurovascular imaging such as CT or M-R angiography or carotid ultrasound, cardiac monitoring for atrial fibrillation, echocardiography for left heart thrombus or patent foramen ovale, and routine blood tests.
Emergent Vascular Imaging:
Patients with high-risk TIAs (ABCD2 score greater or equal to 4) or crescendo symptoms should undergo immediate vascular imaging (CT or M-R angiography) to identify carotid stenosis or intracranial thrombus amenable to urgent intervention. This can significantly reduce stroke risk if done within 24 hours. The ABCD2 Score considers age, blood pressure, clinical features, duration, and diabetes mellitus, to predict stroke risk accurately at 2, 7, and 90 days post-TIA.
Antiplatelet Therapy:
Patients with TIA should receive dual antiplatelet therapy (aspirin plus clopidogrel) for the first 21 days, as this confers the greatest stroke risk reduction during the highest risk period. After 21 days, monotherapy is recommended to mitigate bleeding risk.
TIA Mimics:
Clinicians must distinguish true TIAs from other transient neurological events like migraines, seizures, or metabolic encephalopathies that may resemble TIAs. TIA symptoms are negative (loss of function) rather than positive phenomena like headaches or visual auras seen in migraines. The history, tempo of symptom evolution, and presence of positive phenomena like headaches can help differentiate mimics.
Visual Symptoms:
Particular attention should be paid to patients presenting with visual field deficits or monocular blindness, which are often wrongly attributed to ophthalmological causes. These may represent retinal TIAs or strokes, carrying high future stroke risk if not properly investigated.
Cardiac Evaluation:
All TIA patients require screening for atrial fibrillation via ECG, prolonged cardiac monitoring, and echocardiography if indicated. The presence of atrial fibrillation is a major risk factor for embolic stroke, necessitating long-term anticoagulation.
Secondary Stroke Prevention:
Following a TIA, patients require aggressive medical therapy to prevent future strokes. This includes antiplatelet or anticoagulant therapy, treatment of hypertension, hyperlipidemia, diabetes, smoking cessation, and lifestyle modifications.
In summary, TIAs mandate urgent evaluation and management to mitigate the high short-term risk of disabling ischemic stroke. Thorough diagnostic workup, emergent vascular imaging, appropriate antithrombotic therapy, and rapid implementation of secondary prevention measures are essential to optimize patient outcomes.