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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.
- 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 (see “ ” and “ ”) and etiology. 
- Atypical symptoms may be seen. 
- Features suggesting a specific underlying cause
Perform a full physical examination to assess for neurological deficits and look for evidence of specific causes.
The differential diagnoses listed here are not exhaustive.
- Establish a , focusing on , their onset, and changes over time.
- Obtain an immediate ECG and point-of-care glucose.
- Rule out alternate diagnoses, e.g., acute ischemic stroke or (see “”).
Complete , i.e., laboratory studies, neuroimaging, and cardiac evaluation, within 24–48 hours of symptom onset to:
- Identify the etiology
- Ensure timely stroke prevention 
- Perform .
- Treating the underlying etiology
- Other prevention measures, e.g.,
Disposition is decided based on clinical judgment, as there is no evidence-based consensus. 
Neurology consultation is recommended for:
- Patients with complex or high-risk TIAs requiring admission
- All patients in follow-up to help tailor long-term stroke prevention
- Use clinical scoring systems as a guide only (see “Risk stratification”). 
- Features that support admission include: 
- Multiple TIA episodes or TIA while on therapeutic anticoagulation
- Evidence of a potential embolic source
- Inability to complete outpatient workup within 2 days
- If discharged from the emergency department:
- Advise patients to return if symptoms recur.
- Prescribe as indicated.
- Ensure outpatient follow-up.
Risk scoring systems and imaging findings do not replace clinical judgment in determining overall stroke risk and disposition.
Laboratory studies 
- Immediate: serum glucose
- Subsequent (within 24–48 hours of presentation)
- risk factors or identifiable cause.  : Consider after initial diagnostic findings, notably in younger patients with TIA and no vascular
- 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). 
- Indications: all patients within 24–48 hours of presentation 
- Choice of modality and sequence: depends on whether there is clinical suspicion of and available resources; follow local protocols and consult a neurologist as needed.
Neurovascular studies in TIA 
- 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. 
- Supportive findings
Cardiac evaluation 
- All patients: ECG to evaluate for atrial fibrillation, atrial flutter, or another concomitant cardiac condition
Patients with suspected embolic source or unknown etiology: Further cardiac evaluation is indicated. 
- atrial fibrillation  : to detect occult
- 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. 
- The Canadian TIA score can be used to assess the 7-day risk of stroke. 
|ABCD2 score |
≥ 60 years
|Blood pressure|| |
|Clinical features|| |
Speech impairment only
|Duration of symptoms|| |
≥ 60 minutes
|Diabetes mellitus|| |
The ABCDE2 score is only a general guide; it cannot reliably identify low-risk patients who can be discharged from ambulatory settings in isolation. 
High-risk imaging findings
- Findings of high early stroke risk require rapid assessment and early secondary prevention measures.
- High-risk imaging findings include:
Antithrombotic therapy for TIA 
- Indication: most patients with no and/or antiplatelet agents 
- Choice of agent: based on patient risk, underlying etiology, and existing medications; prescribe in consultation with a specialist.
- Timing of therapy: preferably within 24 hours and after ruling out ICH 
- Risk assessment: Balance the risk of subsequent stroke with the risk of bleeding from therapy (see, e.g., “ ” and “ ”).
Antiplatelets are generally preferred over oral anticoagulation. 
- Low-risk TIA
- High-risk TIA (ABCD2 ≥ 4 or according to clinician assessment): Consult neurology.
The choice of agents and dosage is based on the etiology and clinical manifestation, e.g.:
- Atrial fibrillation or atrial flutter: typically anticoagulation, usually with DOACs (see “ ” for details)
- Valvular disease: Recommendations depend on valve pathology. 
Large artery disease
The choice of agents and dosage is based on the etiology and clinical severity, e.g.:
Carotid artery stenosis
- Antiplatelet monotherapy is typically prescribed initially.
- See “ ” for details.
Cervical artery dissection 
- Antiplatelet therapy or anticoagulation may be prescribed.
- See “ ” for details.
- See also “ .”
Can manifest as cardioembolic or noncardioembolic TIA. The choice of agents and dosage is based on the etiology and clinical manifestation, e.g.:
- Antiplatelet therapy and/or anticoagulation may be indicated.
- See “ ” for details.
Consider as a cause of TIA in young female patients with no . 
Patients already on antithrombotic therapy
- Currently on antiplatelet monotherapy
- Chronic anticoagulation
Surgical or intravascular intervention 
- Indications include certain severe forms of or .
- See “ ” for details.
Long-term stroke prevention
- Determine the time of symptom onset and resolution.
- Establish IV access.
- Perform immediate ECG and POC glucose.
- Order initial laboratory studies.
- Perform immediate neuroimaging to rule out acute infarct and alternative diagnoses.
- Stratify the risk of stroke and determine appropriate disposition.
- Consider immediate antiplatelet therapy (see antithrombotic therapy for TIA).
- Complete appropriate neurovascular studies within 24–48 hours of admission.
- Consider further cardiology studies.
- Initiate secondary prevention measures according to the underlying etiology.
- Address modifiable risk factors.
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.
Increased risk of future ischemic stroke 
- Within 2 days: ∼ 3–10%
- Within 90 days: ∼ 9–17%