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Emergency and Acute Medicine – Transient Ischemic Attack (TIA)
A transient ischemic attack (TIA) is a brief episode of neurologic dysfunction caused by a temporary reduction in blood flow to a region of the central nervous system. Traditionally defined as symptoms lasting less than 24 hours, most TIAs resolve within one hour. Importantly, TIA is a major warning sign for impending stroke, with approximately 12–30% of strokes preceded by a TIA.
The underlying mechanism involves transient cerebral hypoperfusion. Common causes include atherosclerotic thrombosis in large or medium arteries, small vessel disease, and emboli originating from the heart—particularly in conditions such as Atrial fibrillation. Less common causes include arterial dissection, vasculitis, and hypercoagulable states, while in a significant proportion of patients, no clear etiology is identified.
Clinical presentation depends on the vascular territory affected. Large-vessel TIAs produce characteristic focal deficits. For example, involvement of the middle cerebral artery causes contralateral weakness and sensory loss affecting the face and arm more than the leg, often accompanied by aphasia (dominant hemisphere) or neglect (nondominant hemisphere). Posterior circulation TIAs may present with vertigo, ataxia, diplopia, or cranial nerve deficits. Transient monocular blindness, known as amaurosis fugax, reflects involvement of the ophthalmic branch of the internal carotid artery. Small-vessel (lacunar) TIAs typically produce isolated motor or sensory deficits without cortical signs.
The history is critical in diagnosis. TIAs typically have sudden onset, short duration, and produce “negative” neurologic symptoms such as weakness, vision loss, or aphasia due to loss of function. In contrast, gradual onset or “positive” symptoms such as tingling, jerking, or visual scintillations suggest alternative diagnoses like migraine or seizure.
Physical examination should include a detailed neurologic assessment, evaluating strength, sensation, coordination, speech, and visual fields. By definition, neurologic deficits resolve in TIA; persistent deficits indicate an acute Ischemic stroke rather than TIA. Standardized tools such as the NIH Stroke Scale can aid in assessment and monitoring.
Initial evaluation in the emergency setting focuses on excluding mimics and identifying risk factors. A rapid bedside glucose test is essential, as hypoglycemia can mimic focal neurologic deficits. A noncontrast CT scan of the head should be obtained urgently to exclude intracranial hemorrhage. MRI with diffusion-weighted imaging is more sensitive and may reveal infarction in up to 50% of patients initially thought to have TIA. Vascular imaging of the head and neck—via CT angiography, MR angiography, or carotid ultrasound—is important, as nearly half of patients have significant arterial stenosis or occlusion.
Additional workup includes ECG to detect arrhythmias such as atrial fibrillation and echocardiography to evaluate for cardiac sources of emboli. Laboratory tests assess metabolic abnormalities,
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