Transient ischemic attack

Last updated: September 23, 2021

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Transient ischemic attack (TIA) is a temporary, focal cerebral ischemic event that results in reversible neurological symptoms but is not associated with a visible acute infarct on neuroimaging. Cardiogenic embolism (e.g., from atrial fibrillation) and atherosclerosis (e.g., carotid artery stenosis) are the most commonly identified etiologies. Symptoms depend on the affected territory and may mimic an acute stroke; however, symptoms are transient. Because patients with TIA have an increased stroke risk, early diagnosis and initiation of secondary preventive therapies for subsequent stroke are vital. Management typically includes urgent neuroimaging, antithrombotic therapy (e.g., antiplatelet therapy), and prompt determination of the underlying cause (e.g., using echocardiography and neurovascular studies) to guide targeted preventative measures, such as the management of underlying atrial fibrillation or carotid artery stenosis. See also ischemic stroke and overview of stroke.

TIA refers to temporary, focal cerebral ischemia that results in reversible neurologic deficits without acute infarction (i.e., imaging findings show no signs of infarction). [1]

See differential diagnoses of stroke.

The differential diagnoses listed here are not exhaustive.


If there is evidence of an acute infarct on imaging, start immediate management for an acute ischemic stroke.

General principles

  • TIA is a clinical diagnosis (see “Clinical features” section).
  • The diagnostic evaluation for suspected TIA is similar to that for acute ischemic stroke (see “Diagnosis of ischemic stroke”).
  • Ruling out alternate diagnoses and early determination of etiology are key parts of the evaluation.
  • Start the workup as soon as possible following symptom onset and within 24 hours of patient presentation. [8][10]

Laboratory studies [8][10]

  • Immediate: serum glucose
  • Subsequent (within 24 hours of presentation)
  • Optional
    • Hypercoagulable workup: Consider after initial diagnostic findings, notably in younger patients with TIA and no vascular risk factors or identifiable cause. [1][8]
    • Toxicological screen (e.g., urine drug screen, blood alcohol level): Consider if there is clinical suspicion for drug intoxication (e.g., physical signs, history of substance misuse). [11][12]

Neuroimaging [8][10]

Neuroimaging is indicated for all patients with suspected TIA within 24 hours of presentation to rule out acute cerebral infarct (i.e., ischemic stroke).

Head CT (without IV contrast)

MRI brain

  • Indication: DW-MRI is the recommended imaging modality for a suspected TIA. [8]
  • Supportive findings

A brain MRI is preferred for TIA evaluation, but a head CT (without IV contrast) must be performed first and immediately if there is concern for hemorrhage or acute infarction requiring reperfusion therapy.

Neurovascular studies in TIA [8][10]

  • Indication: all patients with a suspected TIA to determine the etiology and guide secondary prevention measures
  • Timing: ideally within 24 hours
  • Imaging: Modality is chosen based on patient factors and institutional preferences. [8]
  • Supportive findings

Cardiac evaluation [8][10]

General considerations

  • Estimating the patient's risk of a future stroke after a TIA helps guide management decisions (e.g., further diagnostic workup, treatment, and disposition).
  • Individual risk depends on a combination of clinical and diagnostic parameters.
  • Risk score reliability remains limited and a complete clinical risk assessment is recommended.

Clinical scoring systems

The ABCD2 risk assessment score is most frequently used to assess short-term stroke risk. [15][16][17][18]

ABCD2 score [19]
Criteria Points

≥ 60 years


Blood pressure

SBP ≥ 140 mm Hg OR DBP ≥ 90 mm Hg


Clinical features

Speech impairment only


Unilateral weakness


Duration of symptoms

10–59 minutes


≥ 60 minutes


Diabetes mellitus




  • Score 0 to 3: low two-day stroke risk (1%)
  • Score 4 to 5: moderate two-day stroke risk (4%)
  • Score 6 to 7: high two-day stroke risk (8%)

High-risk imaging findings

Disposition [8][17]

Hospitalization should be considered for patients with suspected TIA within 72 hours of onset PLUS any of the following:

  • ABCD2 score: ≥ 3
  • ABCD2 score: 0 to 2 PLUS inability to complete outpatient workup within 2 days
  • ABCD2 score: 0 to 2 PLUS other evidence that the event was caused by focal ischemia
  • High early stroke risk or need for intervention according to clinician judgment

General principles

  • There is no specific treatment for the TIA itself.
  • Therapeutic goals consist of preventing subsequent stroke (i.e., secondary prevention) and treatment of underlying conditions.
  • For primary prevention measures that decrease the likelihood of a first TIA, see “Prevention” in ischemic stroke.

Antithrombotic therapy for TIA [1][10][21]

  • Choice of agent should take the following into consideration:
    • Preventative pharmacotherapy the patient was taking at the time of the TIA event
    • TIA severity (and risk of subsequent ischemic stroke)
    • Suspected etiology
    • Patient comorbidities
  • Timing: within 24 hours (start as soon as safely possible after establishing ischemic diagnosis and ruling out hemorrhage) [22]
Initial stroke prevention therapy in TIA [1][10][21][23]
Preventative stroke medication prior to TIA event Stroke prevention therapy
  • Low-risk TIA: aspirin [1]
  • High-risk TIA : Consider DAPT for 21 days with aspirin AND clopidogrel in consultation with neurology. [1][23]
  • Known cardioembolic source or indication for anticoagulation : Initiate anticoagulation therapy.
Antiplatelet monotherapy
  • Consider changing to DAPT with aspirin AND clopidogrel in consultation with neurology. [1][23]
  • Known cardioembolic source or indication for anticoagulation : Initiate anticoagulation therapy and reassess the indication for continued antiplatelet therapy. [1]
Chronic anticoagulation
  • Ensure therapeutic dosing of anticoagulant.
  • Consider the risk versus benefit of adding antiplatelet monotherapy if underlying atherosclerosis is likely.

Avoid triple therapy (DAPT plus anticoagulation) because of the increased risk of hemorrhage. [1]

Long-term stroke prevention based on suspected etiology [1][10]

Therapy should be tailored to the suspected underlying etiology.

Management of other modifiable risk factors [1]

See “ASCVD prevention” for detailed information.

A brain MRI is preferred for TIA evaluation but a head CT (without IV contrast) must be performed first and immediately if there is concern for hemorrhage or acute infarction requiring reperfusion therapy.

If there is evidence of an acute infarct on imaging, start immediate management for an acute ischemic stroke.

  • Increased risk of future ischemic stroke [3]
    • Within 2 days: ∼ 3–10%
    • Within 90 days: ∼ 9–17%
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