Transient ischemic attack

To see contributor disclosures related to this article, hover over this reference: ^[1]

Physicians may earn CME/MOC credit by searching for an answer to a clinical question on our platform, reading content in this article that addresses that question, and completing an evaluation in which they report the question and the impact of what has been learned on clinical practice.

AMBOSS designates this Internet point-of-care activity for a maximum of 0.5 AMA PRA Category 1 Credit(s)™. Physicians should claim only credit commensurate with the extent of their participation in the activity.

For answers to questions about AMBOSS CME, including how to redeem CME/MOC credit, see "Tips and Links" at the bottom of this article.

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,” “Overview of stroke,” and “Carotid artery stenosis.”

TIA refers to temporary, focal cerebral ischemia that results in reversible neurological deficits without acute infarction (i.e., imaging findings show no signs of infarction). ^[2][3]

• Prevalence: ∼ 2.3% ^[4][5][6]
• Incidence ^[5]
  • Increases with age
  • ♂ > ♀
• Risk factors: same as those for acute ischemic stroke (see “Risk factors” in “Ischemic stroke”)

• See “Etiology” in “Ischemic stroke.”
• Classification ^[7]
  • Cardioembolic (e.g., due to atrial fibrillation)
  • Lacunar/small vessel disease (e.g., due to chronic hypertension)
  • Large vessel disease/low-flow state (e.g., atherosclerosis of MCA, severe carotid artery stenosis)
  • Blood disorders/hypercoagulable states

• Neurological manifestations
  • 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 “Stroke symptoms by affected vessels” and “Stroke symptoms by affected region”) and etiology. ^[8]
    • Embolic: often a single, discrete episode lasting hours rather than minutes
    • Lacunar stroke/small vessel disease: See “Lacunar syndromes.”
    • Large vessel disease/low-flow state: often recurrent episodes lasting minutes
  • Atypical symptoms may be seen. ^[9]
• Features suggesting a specific underlying cause
  • Atrial fibrillation: palpitations, irregular heart rate
  • Carotid artery stenosis: carotid bruit
  • Endocarditis: fever, heart murmur, history of IV drug abuse
  • Aortic dissection: chest pain, hypotension
  • Paradoxical embolism: features of DVT

Perform a full physical examination to assess for neurological deficits and look for evidence of specific causes.

• See “Differential diagnoses of stroke.”

The differential diagnoses listed here are not exhaustive.

TIA is a self-limiting event that is most often diagnosed retrospectively and requires no specific treatment. The primary management goal is stroke prevention.

Approach ^[2][3][10]

• Establish a clinical diagnosis, focusing on symptoms of TIA, 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 stroke mimics (see “Diagnosis of ischemic stroke”).
• Complete TIA diagnostics, i.e., laboratory studies, neuroimaging, and cardiac evaluation, within 24–48 hours of symptom onset to:
  • Identify the etiology
  • Ensure timely stroke prevention ^[2][11]
• Perform TIA risk stratification.
• Reduce subsequent stroke risk through:
  • Antithrombotic therapy for TIA
  • Treating the underlying etiology
  • Other prevention measures, e.g., ASCVD prevention

Treat patients with ongoing neurological deficits or acute infarct seen on imaging as having an acute stroke; see “Initial management of acute stroke.”

Disposition ^[3][11]

Disposition is decided based on clinical judgment, as there is no evidence-based consensus. ^[11][12][13]

• 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”). ^[3]
• Features that support admission include: ^[11][12]
  • 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 antithrombotic therapy for TIA 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 ^[2][3][10]

• Immediate: serum glucose
• Subsequent (within 24–48 hours of presentation)
  • CBC
  • BMP
  • Coagulation panel
  • Serum troponin
  • Serum lipid panel ^[10]
  • HbA1c
• Optional
  • Hypercoagulability workup: Consider after initial diagnostic findings, notably in younger patients with TIA and no vascular risk factors or identifiable cause. ^[3][14]
  • 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). ^[15][16]

Neuroimaging ^[2][3][10]

• Indications: all patients within 24–48 hours of presentation ^[2]
• Choice of modality and sequence: depends on whether there is clinical suspicion of hemorrhagic stroke and available resources; follow local protocols and consult a neurologist as needed.
  • Noncontrast CT head
    • Rapidly rules out intracranial hemorrhage and is readily available at most centers
    • If required, neurovascular studies for TIA can be included.
  • MRI brain
    • More sensitive than CT for ischemic stroke
    • Diffusion-weighted imaging is preferred. ^[11]
    • Can be performed after or instead of CT head
  • See “Stroke neuroimaging” for details.
• Findings
  • Typically normal or no acute findings
  • Old infarcts or chronic ischemic changes may be seen.

Neurovascular studies in TIA ^[2][3][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. ^[3]
  • CTA head and neck
  • MRA head and neck
  • Carotid Doppler ultrasound ^[11][17]
  • Transcranial Doppler
• Supportive findings
  • Carotid artery stenosis
  • Intra- or extracranial stenotic atherosclerotic lesion
  • Intracranial embolic lesion
  • Arterial dissection

Cardiac evaluation ^[2][3][10]

• 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. ^[18]
  • Echocardiography
    • TTE is preferred.
    • Consider TEE if identification of a PFO , valvular disease, or aortic arch atherosclerosis will change management. ^[3]
    • Supportive findings
      • Left atrial or ventricular thrombus
      • Dilated or restrictive cardiomyopathy
      • Patent foramen ovale (PFO)
      • Cardiac tumor
  • Ambulatory ECG monitoring: to detect occult atrial fibrillation ^[2]

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. ^{[11][19][20][21]}
• The Canadian TIA score can be used to assess the 7-day risk of stroke. ^[22]

The ABCDE² score is only a general guide; it cannot reliably identify low-risk patients who can be discharged from ambulatory settings in isolation. ^[11]

High-risk imaging findings

• Findings of high early stroke risk require rapid assessment and early secondary prevention measures.
• High-risk imaging findings include:
  • Distal vertebral and proximal basilar artery lesion ^[17]
  • Distal basilar artery and middle cerebral artery lesion
  • Severe carotid artery stenosis ^[2]
  • Cerebral or cervical arterial dissection (see “Dissection of the carotid and the vertebral artery”) ^[24]

Antithrombotic therapy for TIA ^{[2][10][14][25]}

• Indication: most patients with no contraindications to anticoagulation and/or antiplatelet agents ^[2][26]
• Choice of agent: based on patient risk, underlying etiology, and existing medications; prescribe in consultation with a specialist.
  • Single antiplatelet agents (e.g., aspirin, clopidogrel): most common
  • Dual antiplatelet therapy (DAPT): used for short-term therapy in select patients
  • Anticoagulants (e.g., VKAs, DOACs): indicated for specific underlying etiologies (e.g., atrial fibrillation); usually not combined with antiplatelet therapy
• Timing of therapy: preferably within 24 hours and after ruling out ICH ^[2][11][26]
• Risk assessment: Balance the risk of subsequent stroke with the risk of bleeding from therapy (see, e.g., “HAS-BLED score” and “Risk of major bleeding from anticoagulation”).

Noncardioembolic TIA

Antiplatelets are generally preferred over oral anticoagulation. ^[2]

• Low-risk TIA
  • Aspirin ^[2]
  • OR clopidogrel ^[2]
  • OR combination extended-release dipyridamole/aspirin ^[2]
• High-risk TIA (ABCD² ≥ 4 or according to clinician assessment): Consult neurology.
  • Start DAPT, e.g., aspirin PLUS clopidogrel , within 1–7 days. ^[2][14][27]
  • Continue for 21–90 days then switch to antiplatelet monotherapy.

Avoid triple therapy (i.e., combined DAPT and anticoagulation) or prolonged DAPT (i.e., > 90 days) in patients with noncardioembolic TIA, because of the risk of hemorrhage. ^[2]

Cardioembolic TIA

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 “Anticoagulation for atrial fibrillation” for details)
• Valvular disease: Recommendations depend on valve pathology. ^[2]

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 “Management of carotid artery stenosis” for details.
• Cervical artery dissection ^[2]
  • Antiplatelet therapy or anticoagulation may be prescribed.
  • See “Carotid and vertebral artery dissection” for details.
  • See also “Cerebrovascular fibromuscular dysplasia.”

Hypercoagulable states

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 “Treatment of hypercoagulable states” for details.

Consider antiphospholipid syndrome as a cause of TIA in young female patients with no ASCVD risk factors. ^[28]

Patients already on antithrombotic therapy

• Currently on antiplatelet monotherapy
  • Consider switching to DAPT in consultation with neurology. ^[2]
  • Patients with indications for anticoagulation (e.g., Afib): Consider switching to or adding anticoagulation. ^[14]
• Chronic anticoagulation
  • Ensure therapeutic dosing of oral anticoagulants.
  • Consult a specialist (e.g., neurology, cardiology) to determine if the addition of antiplatelet monotherapy is indicated.

Surgical or intravascular intervention ^[2]

• Indications include certain severe forms of carotid artery stenosis or cervical artery dissection.
• See “Carotid revascularization” for details.

Long-term stroke prevention

• Management depends on:
  • Underlying etiology: e.g., large-vessel disease, cardioembolic sources, hypercoagulable states, atherosclerosis
  • Patient risk factors: ASCVD risk factors, lifestyle, perioperative risk assessment (e.g., for carotid endarterectomy)
• See “Reducing subsequent stroke risk” and “ASCVD prevention” for details.

• 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.
  • Low risk: Schedule appropriate outpatient studies prior to discharge.
  • High risk: Admit to hospital under internal medicine or neurology service.
• 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.

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

• Increased risk of future ischemic stroke ^[5]
  • Within 2 days: ∼ 3–10%
  • Within 90 days: ∼ 9–17%