A transient ischemic attack (TIA) represents focal brain ischemia that reverses before leaving a permanent neurologic deficit. Most TIAs present suddenly and last for minutes, though on occasion symptoms can persist or fluctuate for hours before recovery. Given the transient nature of the symptoms, initial suspicion for TIA often depends on the patient’s description of the event. This may be imprecise depending on the patient’s ability to accurately describe symptoms; a high level of suspicion for TIA is therefore always appropriate. TIA represents a warning sign of possible impending stroke, with the first 48 hours the highest risk period. Start antiplatelet therapy immediately and perform a diagnostic evaluation to determine the underlying mechanism that will guide long-term preventative therapy.
There are a number of nonvascular causes of transient neurologic symptoms. The most important are seizure with transient postictal deficits (usually apparent from the history), and migrainous phenomenon. Use care in making the latter diagnosis, as headache may also accompany TIA; a history of migraine with aura along with similar stereotyped events in the past argues for migraine as a cause. When the diagnosis is uncertain, it is generally advisable to pursue a TIA workup to ensure a vascular cause is not responsible for the episode.
Head computed tomography (CT) is commonly the initial imaging study. Rarely, patients with brain tumors or small subdural hematomas will present with transient focal neurologic symptoms, and these will generally be seen on CT. Magnetic resonance imaging (MRI) of the brain is a more sensitive test to identify acute ischemic changes (see section E), but in most centers is not easily and/or rapidly available.
If urgent vascular imaging is performed and shows large artery atherosclerotic disease, or if this is known to exist prior to the TIA, the short-term risk of stroke is substantially increased and aggressive therapy is appropriate (see section F).
The ABCD 2 score is a risk stratification tool that can be used to estimate the risk of stroke following TIA. It can be quickly calculated during the initial evaluation. A score of 0–3 suggests a 48-hour stroke risk of about 1%; higher scores are associated with higher risk of up to 10% in the first 48 hours.
MRI brain with diffusion-weighted imaging (DWI) sequences reveals acute infarction in about one-third of TIA patients. When present, the diagnosis of a vascular cause is confirmed and evaluation should proceed as for those with stroke; further, the risk of subsequent stroke is substantially greater. A negative MRI DWI study does not rule out TIA, but given the lower risk of future stroke and, in many cases, uncertainty about whether a vascular cause was responsible for symptoms, a more conservative evaluation for underlying etiology may be reasonable. MRI may also reveal an alternative diagnosis, such as tumor or demyelination. In patients with an obvious cause for TIA, such as atrial fibrillation or carotid stenosis, MRI may not be necessary.
In high-risk patients (ABCD 2 score ≥ 4 or large artery disease) who present within 24 hours, dual antiplatelet therapy with aspirin and clopidogrel lowers the risk of recurrent stroke and should be administered as soon as possible. A loading dose of both (aspirin 162–325 mg, clopidogrel 300–600 mg) should be given, followed by a 21-day course of treatment. After this, antiplatelet monotherapy should be continued indefinitely. If subsequent evaluation reveals a cardioembolic source warranting anticoagulation (e.g., atrial fibrillation), dual antiplatelet therapy should be discontinued and replaced with oral anticoagulation.