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Transient ischemic attack (TIA)


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]



Differential diagnoses

See differential diagnoses of stroke.

The differential diagnoses listed here are not exhaustive.

Clinical features

  • Acute, transient focal neurologic symptoms
  • Typically, symptoms last < 1 hour (the majority of cases resolve in < 15 minutes).
  • Symptoms depend on the affected territory (see stroke symptoms by affected vessels and stroke symptoms by affected region) and etiology. [6]
    • Embolic: often a single, discrete episode lasting hours rather than minutes
    • Lacunar/small vessel disease: Symptoms usually resemble those seen in lacunar stroke.
    • Large vessel disease/low-flow state: often recurrent episodes lasting minutes
  • Atypical symptoms may be seen. [7]



  • Perform an initial clinical evaluation , immediate ECG, and point-of-care glucose.
  • Complete laboratory studies and neuroimaging (within 24 hours of symptom onset). [8][9]
  • Stratify the risk of subsequent stroke (see “Risk stratification” section).
  • Identify and treat the underlying etiology.
  • Initiate stroke prevention measures (e.g., antiplatelet agents).
  • 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

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. [10][8]

Laboratory studies [10][8]

  • 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. [8][1]
    • 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 [10][8]

Neuroimaging is indicated for all patients with suspected TIA within 24 hours of presentation to rule out acute infarct.

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 [10][8]

  • 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]
    • CTA head and neck
    • MRA head and neck
    • Transcranial doppler/carotid duplex ultrasound (TCD/CUS) [13]
  • Supportive findings

Cardiac evaluation [8][10]

Risk stratification

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 [17][8]

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


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 [10][1][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 [10][1][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 [10][1]

Therapy should be tailored to the suspected underlying etiology.

Management of other modifiable risk factors [1]

  • Diabetes screening and treatment
  • Obesity screening and lifestyle counseling
  • Physical activity counseling
  • Consider nutritionist consultation or assessment. [24]
  • Consider obstructive sleep apnea (OSA) screening. [10]
  • Smoking cessation and elimination/reduction of alcohol intake

Acute management checklist

  • 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 alternate 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 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 [3]
    • Within 2 days: ∼ 3–10%
    • Within 90 days: ∼ 9–17%
  • 1. Kernan WN, Ovbiagele B, Black HR et al. Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack. Stroke. 2014; 45(7): pp. 2160–2236. doi: 10.1161/STR.0000000000000024.
  • 2. Johnston SC, Fayad PB, Gorelick PB, et al. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. 2003; 60(9): pp. 1429–1434. doi: 10.1212/01.wnl.0000063309.41867.0f.
  • 3. Virani SS, Alonso A, Benjamin EJ, et al. Heart Disease and Stroke Statistics—2020 Update: A Report From the American Heart Association. url: http://dx.doi.org/10.1161/CIR.0000000000000757 Accessed August 5, 2020.
  • 4. Degan D, Ornello R, Tiseo C, et al. Epidemiology of Transient Ischemic Attacks Using Time- or Tissue-Based Definitions. Stroke. 2017; 48(3): pp. 530–536. doi: 10.1161/strokeaha.116.015417.
  • 5. Al-Khaled M, Eggers J. MRI findings and stroke risk in TIA patients with different symptom durations. Neurology. 2013; 80(21): pp. 1920–1926. doi: 10.1212/wnl.0b013e318293e15f.
  • 6. Kimura K, Minematsu K, Yasaka M, Wada K, Yamaguchi T. The duration of symptoms in transient ischemic attack. Neurology. 1999; 52(5): pp. 976–976. doi: 10.1212/wnl.52.5.976.
  • 7. Paul NL, Simoni M, Rothwell PM. Transient isolated brainstem symptoms preceding posterior circulation stroke: a population-based study. The Lancet Neurology. 2013; 12(1): pp. 65–71. doi: 10.1016/s1474-4422(12)70299-5.
  • 8. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. Stroke. 2009; 40(6): pp. 2276–93. doi: 10.1161/STROKEAHA.108.192218.
  • 9. Rothwell PM, Giles MF, Chandratheva A, et al. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. The Lancet. 2007; 370(9596): pp. 1432–1442. doi: 10.1016/s0140-6736(07)61448-2.
  • 10. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019; 50(12). doi: 10.1161/str.0000000000000211.
  • 11. EC J, JL S, Jr AH, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke. 2013; 44(3): pp. 870–947. doi: 10.1161/STR.0b013e318284056a.
  • 12. Simmons BB, Cirignano B, Gadegbeku AB. Transient ischemic attack: Part I. Diagnosis and evaluation. Am Fam Physician. 2012; 86(6): pp. 521–6. pmid: 23062043.
  • 13. Gulli G, Khan S, Markus HS. Vertebrobasilar Stenosis Predicts High Early Recurrent Stroke Risk in Posterior Circulation Stroke and TIA. Stroke. 2009; 40(8): pp. 2732–2737. doi: 10.1161/strokeaha.109.553859.
  • 14. Morris JG, Duffis EJ, Fisher M. Cardiac Workup of Ischemic Stroke. Stroke. 2009; 40(8): pp. 2893–2898. doi: 10.1161/strokeaha.109.551226.
  • 15. Merwick Á, Albers GW, Amarenco P, et al. Addition of brain and carotid imaging to the ABCD2 score to identify patients at early risk of stroke after transient ischaemic attack: a multicentre observational study. The Lancet Neurology. 2010; 9(11): pp. 1060–1069. doi: 10.1016/s1474-4422(10)70240-4.
  • 16. Wardlaw JM, Brazzelli M, Chappell FM, et al. ABCD2 score and secondary stroke prevention. Neurology. 2015; 85(4): pp. 373–380. doi: 10.1212/wnl.0000000000001780.
  • 17. Lo BM, Carpenter CR, Hatten BW, et al. Clinical Policy: Critical Issues in the Evaluation of Adult Patients With Suspected Transient Ischemic Attack in the Emergency Department. Ann Emerg Med. 2016; 68(3): pp. 354–370.e29. doi: 10.1016/j.annemergmed.2016.06.048.
  • 18. Perry JJ, Sharma M, Sivilotti MLA, et al. Prospective validation of the ABCD2 score for patients in the emergency department with transient ischemic attack. Can Med Assoc J. 2011; 183(10): pp. 1137–1145. doi: 10.1503/cmaj.101668.
  • 19. Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. The Lancet. 2007; 369(9558): pp. 283–292. doi: 10.1016/s0140-6736(07)60150-0.
  • 20. Lee VH, Brown RD, Mandrekar JN, Mokri B. Incidence and outcome of cervical artery dissection: A population-based study. Neurology. 2006; 67(10): pp. 1809–1812. doi: 10.1212/01.wnl.0000244486.30455.71.
  • 21. Sorensen AG, Ay H. Transient ischemic attack: definition, diagnosis, and risk stratification. Neuroimaging Clin N Am. 2011; 21(2): pp. 303–13, x. doi: 10.1016/j.nic.2011.01.013.
  • 22. Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy--An evidence-based review: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2005; 65(6): pp. 794–801. doi: 10.1212/01.wnl.0000176036.07558.82.
  • 23. Prasad K, Siemieniuk R, Hao Q, et al. Dual antiplatelet therapy with aspirin and clopidogrel for acute high risk transient ischaemic attack and minor ischaemic stroke: a clinical practice guideline. BMJ. 2018; 363: p. k5130. doi: 10.1136/bmj.k5130.
  • 24. Whelton, PK, Carey, RM et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Hypertension. 2017; 71(6): pp. e13–e115. doi: 10.1161/hyp.0000000000000065.
  • DeBaun MR, Jordan LC, King AA, et al. American Society of Hematology 2020 guidelines for sickle cell disease: prevention, diagnosis, and treatment of cerebrovascular disease in children and adults. Blood Advances. 2020; 4(8): pp. 1554–1588. doi: 10.1182/bloodadvances.2019001142.
  • Wong KSL, Chen C, Fu J, et al. Clopidogrel plus aspirin versus aspirin alone for reducing embolisation in patients with acute symptomatic cerebral or carotid artery stenosis (CLAIR study): a randomised, open-label, blinded-endpoint trial. The Lancet Neurology. 2010; 9(5): pp. 489–497. doi: 10.1016/s1474-4422(10)70060-0.
  • Whitlock RP, Sun JC, Fremes SE, Rubens FD, Teoh KH. Antithrombotic and Thrombolytic Therapy for Valvular Disease. Chest. 2012; 141(2): pp. e576S–e600S. doi: 10.1378/chest.11-2305.
  • ACOG Committee on Obstetric Practice. ACOG Committee Opinion No. 743: Low-Dose Aspirin Use During Pregnancy. Obstet Gynecol. 2018; 132(1): pp. e44–e52. doi: 10.1097/AOG.0000000000002708.
  • Murphy SJX, Naylor AR, Ricco J-B, et al. Optimal Antiplatelet Therapy in Moderate to Severe Asymptomatic and Symptomatic Carotid Stenosis: A Comprehensive Review of the Literature. European Journal of Vascular and Endovascular Surgery. 2019; 57(2): pp. 199–211. doi: 10.1016/j.ejvs.2018.09.018.
last updated 10/02/2020
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