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Transient Ischemic Attack

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Last Update: July 17, 2023.

Continuing Education Activity

A transient ischemic attack (TIA) is a medical emergency. It is defined as a transient episode of neurologic dysfunction due to focal brain, spinal cord, or retinal ischemia without acute infarction or tissue injury. Evaluation of TIA should be done urgently with imaging and laboratory studies to decrease the risk of subsequent strokes. Immediate multimodal therapeutic interventions should be initiated. Specific underlying etiology needs to be managed accordingly. This treatment scheme may substantially reduce the risk of recurrent strokes or future TIA by at least 80 percent. This activity examines when this condition should be considered in differential diagnosis and how to evaluate it properly. This activity highlights the role of the interprofessional team in caring for patients with this condition.


  • Describe the pathophysiology of transient ischemic attacks.
  • Review the evaluation of a patient with transient ischemic attacks.
  • Summarize the treatment options for transient ischemic attacks.
  • Outline the importance of enhancing care coordination among the interprofessional team to ensure proper evaluation and management of transient ischemic attacks.
Access free multiple choice questions on this topic.


A transient ischemic attack (TIA) is a medical emergency. It is defined as a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia without acute infarction or tissue injury. The definition of a TIA has moved from time-based to tissue-based. A TIA typically lasts less than an hour, more often minutes. TIA can be considered a serious warning of an impending ischemic stroke; the risk is highest in the first 48 hours following a transient ischemic attack. Differentiating transient ischemic attack from other mimicking conditions is important. Transient ischemic attacks are usually associated with a focal neurologic deficit and/or speech disturbance in a vascular territory due to underlying cerebrovascular disease. It is always sudden in onset. Evaluation of TIA should be done urgently with imaging and laboratory studies to decrease the risk of subsequent strokes. The subsequent risk of TIA or ischemic stroke can be stratified with a simple clinical measure. Immediate multimodality therapeutic interventions should be initiated. These will include aggressive treatment of blood pressure, high-dose statin, antiplatelet therapy, blood sugar control, diet, and exercises. Specific underlying etiology needs to be managed accordingly. This treatment scheme may substantially reduce the risk of recurrent strokes or future TIA by at least 80%.[1][2][3]


TIA subtypes, classified according to the pathophysiological mechanisms, are similar to ischemic stroke subtypes. They include large artery atherothrombosis, cardiac embolism, small vessel (lacunar), cryptogenic, and uncommon subtypes such as vascular dissection, vasculitis, etc. The common risk factors for all TIA include diabetes, hypertension, age, smoking, obesity, alcoholism, unhealthy diet, psychosocial stress, and lack of regular physical activity. A previous history of stroke or TIA will increase substantially the subsequent risk of recurrent stroke or TIA.[4][5] Among all risk factors, hypertension is the most important one for an individual as well as in a population.


TIA incidence in a population is difficult to estimate due to other mimicking disorders, but TIA incidence in the United States could be around half a million per year, and estimates are about 1.1 per 1000 in the United States population. The estimated overall prevalence of TIA among adults in the United States is approximately 2%. It has been shown that previous stroke history increases the prevalence of TIA. Few studies have shown that the majority of people who presented with initial stroke had prior TIA symptoms.[4]


The pathophysiology of TIA depends on the subtype as follows. The common issue is the transient interruption of arterial blood flow to an area of the brain supplied by that particular artery.

  • Large artery atherothrombosis. This may be intracranial or extracranial atherothrombosis. The mechanism may be a lack of blood flow distal to the site of arterial stenosis or an artery-to-artery embolism, the more common mechanism.
  • Small vessel ischemic diseases. The underlying pathology is either lipohyalinosis or small vessel arteriolosclerosis. The commonest risk factor is hypertension, followed by diabetes and age.
  • Cardiac embolism. A clot in the cardiac chamber, most commonly in the left atrium, is secondary to atrial fibrillation.
  • Cryptogenic. This is usually a cortical pattern of ischemia without any identifiable large artery atherothrombosis or cardiac source of emboli. More recently it is often referred to as ESUS (embolic stroke of unknown source).
  • Other uncommon causes such as arterial dissection or hypercoagulable states. 

History and Physical

TIA symptoms have often resolved by the time the patient presents to her doctor or emergency department. The history of present illness should include onset, duration, timing, complete neurological symptoms, associated symptoms, and any aggravating or relieving factors. The clinician should also try to identify the associated risk factors such as coronary artery disease, smoking, drug abuse, obesity, diabetes mellitus, dyslipidemia, and hypertension, as well as personal or family history of hypercoagulability disorders, stroke, or TIA. The history should include etiological clues such as a history of atrial fibrillation and recent myocardial infarction to suggest a cardioembolic source; transient loss of vision like a curtain rising or descending will suggest an internal carotid artery problem. The presence of any cortical symptoms, such as language disturbance or visual field loss, will point to a cortical TIA rather than a lacunar syndrome. 

Physical examination should focus on identifying focal neurological deficits and speech disturbances, which are the most common presenting symptoms in patients with TIA. Cranial nerve examination can yield findings of monocular blindness, disconjugate gaze, facial droop, hemianopia, diplopia, abnormal tongue movement, difficulty swallowing, and auditory dysfunction. Some of the motor findings include unilateral weakness in the upper or lower extremities, face, and tongue, increased tone, clonus, rigidity and also abnormal reflexes that could occur with TIA. Cardiac examination and carotid auscultation for a carotid bruit are very important. Fundoscopy is important to look for any fundoscopic evidence of vascular changes as a result of hypertension or diabetes. It may also show a Hollenhorst plaque, which will indicate an underlying internal carotid artery disease.


The goals of the evaluation of TIA are

  1. To prove the vascular origin of the symptoms either directly or indirectly. This means to find evidence of hypoperfusion and/or acute infarction or identify a presumptive source such as a large-vessel stenosis.
  2. To exclude an alternative nonischemic origin
  3. To determine the underlying vascular mechanism, for example, large-vessel atherothrombotic, cardioembolic, and small-vessel lacunar. This determination allows for selecting the optimal therapy for secondary prevention of TIA pr stroke.
  4. To identify prognostic outcome categories.

The 2009 AHA/ASA guidelines include "neuroimaging within 24 hours of symptom onset and further recommend MRI and diffusion-weighted MR imaging as preferred modalities." A head CT, preferably with a CT angiogram, is recommended if an MRI cannot be performed. Brain MRI with diffusion-weighted imaging has a greater sensitivity than CT for detecting small infarcts in patients with TIA. The practitioner should assess the patient's cervicocephalic vasculature for atherosclerotic lesions using carotid ultrasonography/transcranial Doppler ultrasonography, magnetic resonance angiography, or CT angiography. These lesions are treatable. In candidates for carotid endarterectomy, carotid imaging should be performed within 1 week of the onset of symptoms. Cardiac assessment should be done with ECG, Echocardiogram/TEE  to find a cardioembolic source and the presence of patent foramen ovale, valvular disease, cardiac thrombus, and atherosclerosis. Holter monitor or more prolonged cardiac rhythm monitor in the outpatient setting is reasonable for patients with cortical infarction without any clear source of emboli, primarily to evaluate for paroxysmal atrial fibrillation. Routine blood tests, including complete blood count (CBC), PT/INR, CMP, FBS, lipid panel, urine drug screen, and ESR, should be considered.[6][7][5].

National Stroke Association has established guidelines for TIA evaluation as follows in 2006:[8]

CBC = complete blood countCEA = carotid endarterectomyTCD = transcranial Doppler TEE = transesophageal echocardiogramTTE = transthoracic echocardiogram

The ABCD2 score is very important for predicting subsequent risks of TIA or stroke. The ABCD2 score was derived from providing a more robust prediction standard. The ABCD2 score includes age, blood pressure, clinical symptoms, duration, and diabetes.

  • Age: older than 60 years (1 point)
  • Blood pressure greater than or equal to 140/90 mmHg on first evaluation (1 point)
  • Clinical symptoms: a focal weakness with the spell (2 points) or speech impairment without weakness (1 point)
  • Duration greater than 60 min (2 points) or 10 min to 59 min (1 point)
  • Diabetes mellitus (1 point).

The 2-day risk of stroke was 0% for scores of 0 or 1, 1.3% for 2 or 3, 4.1% for 4 or 5, and 8.1% for 6 or 7. Most stroke centers will admit patients with TIA to the hospital for expedited management and observation if the score is 4, 5, or higher. For patients with a lower score, expedited evaluation and management are still warranted. This expedited approach has been proven to improve the outcome.[9]

Treatment / Management

The main aim of treatment of TIA is to decrease the risk of subsequent stroke or TIA. Early treatment after a TIA can significantly reduce the risk of early stroke. Post TIA, the risk of stroke within 3 months has been reported to be around 20%, with approximately 50% of these strokes occurring within the first 2 days after the initial presentation. Evaluating the vessel status and looking for atrial fibrillation when a patient comes with TIA is extremely important. This will significantly reduce future strokes. Management of TIAs should focus on treating underlying etiologies.[10][11][12]

Studies in the new millennium already confirmed the importance of expedited evaluation and treatment plus the polytherapy approach. The EXPRESS study in the UK has shown the importance of early intervention versus regular treatment by reducing 80% of the stroke risk. [13] Hackam et al. did a meta-analysis in 2007 showing that a combination of diet, exercise, antiplatelet, statin, and antihypertensive therapy may reduce the subsequent stroke by 80% to 90%.[14]

More recent studies in China (CHANCE trial) and the multinational POINTE trial also confirmed dual antiplatelet with aspirin and clopidogrel for 3 weeks to 1 month, followed by a single antiplatelet agent, is the best scheme for antiplatelet therapy. [15][16]

The other part of the treatment will depend on the underlying etiology of the TIA. Revascularization is recommended for symptomatic cervical internal carotid artery stenosis of 70% or higher. Carotid endarterectomy may have a slight benefit-to-risk ratio compared with endovascular intervention and stenting. Whether to operate on patients with 50-69% stenosis will depend more on the surgeon's complication rates, given the vast improvement in the efficacy of aggressive medical therapy. The SAPPRIS trial showed that endovascular Wingspan stenting of 70-99% stenosis of intracranial major arterial stenosis is not better than aggressive medical therapy alone. [17]

Oral anticoagulation is indicated for patients with atrial fibrillation or other sources of cardioembolic sources of TIA.

Differential Diagnosis

  • Carotid artery dissection
  • Meningitis
  • Meningococcal meningitis
  • Multiple sclerosis
  • Stroke, ischemic
  • Stroke, hemorrhagic
  • Subarachnoid hemorrhage
  • Syncope


Risk Stratification Scores

Several risk stratification scores have been developed to help physicians manage patients with a TIA. One widely used score is the ABCD2 score:

A= Age more than 60 years / Score 1

B= SBP> 140 or DBP> 90 / Score 1

C= Clinical features:

Speech impairment without weakness / Score 1

Weakness with/without speech impairment / Score 2

D= Duration

More than 60 mins / Score 2

Between 10-59 mins / Score 1

D= Diabetes / Score 1

Patients with an ABCD2 score of 6-7 have an 8% risk of stroke within 48 hours.

Patients with an ABCD2 score of less than 4 have a 1% risk of stroke within 48 hours.

Even though scales are important in the evaluation of TIA, be aware that patients with critical carotid artery stenosis may sometimes present with a very low ABCD2 score.

Pearls and Other Issues

Differentiating other potential causes that mimic TIA is important since diagnosing and treating TIA early can potentially help in preventing a future stroke. Differential diagnosis of TIA includes but is not limited to vertigo, dizziness, seizures, headaches, bells palsy, drug withdrawal, dementia, electrolyte disorders, acute infections, syncope, and alcoholism.

Enhancing Healthcare Team Outcomes

Patients with a TIA often present to the emergency department or the primary caregiver. Because there is a real risk of a severe stroke, it is important that these patients are managed with an interprofessional team of healthcare workers. The triage nurse must be familiar with the symptoms of a TIA and when to call the neurologist. The early risk of stroke varies from 4-9% within 90 days, and without treatment, the risk of a stroke within five years varies from 20-30%. At the same time, these patients also have the same risk factors for adverse cardiac events. Once a TIA has been diagnosed, the patient must be referred to a neurologist. At the same time, the patient should be educated about the importance of blood pressure control, discontinuing smoking, and eating a healthy diet. Finally, the patient should be educated about the symptoms of a stroke and when to seek immediate medical assistance. [18][19] [Level 5]

Review Questions


Gennai S, Giordano-Orsini G, Lefour S, Cuisenier P. [Transient Ischemic Attack: Limits and challenges of early management]. Presse Med. 2018 Nov-Dec;47(11-12 Pt 1):934-937. [PubMed: 30343830]
Yousufuddin M, Young N, Shultz J, Doyle T, Fuerstenberg KM, Jensen K, Arumaithurai K, Murad MH. Predictors of Recurrent Hospitalizations and the Importance of These Hospitalizations for Subsequent Mortality After Incident Transient Ischemic Attack. J Stroke Cerebrovasc Dis. 2019 Jan;28(1):167-174. [PubMed: 30340936]
Kim J, Thrift AG. A Promising Skills-Based Intervention to Reduce Blood Pressure in Individuals With Stroke and Transient Ischemic Attack. JAMA Neurol. 2019 Jan 01;76(1):13-14. [PubMed: 30304354]
Navis A, Garcia-Santibanez R, Skliut M. Epidemiology and Outcomes of Ischemic Stroke and Transient Ischemic Attack in the Adult and Geriatric Population. J Stroke Cerebrovasc Dis. 2019 Jan;28(1):84-89. [PubMed: 30297169]
Cereda CW, Olivot JM. Emergency Department (ED) Triage for Transient Ischemic Attack (TIA). Curr Atheroscler Rep. 2018 Sep 25;20(11):56. [PubMed: 30251027]
Liu L, Ding J, Leng X, Pu Y, Huang LA, Xu A, Wong KSL, Wang X, Wang Y. Guidelines for evaluation and management of cerebral collateral circulation in ischaemic stroke 2017. Stroke Vasc Neurol. 2018 Sep;3(3):117-130. [PMC free article: PMC6169613] [PubMed: 30294467]
Bibok MB, Votova K, Balshaw RF, Penn M, Lesperance ML, Harris DR, Sedgwick C, Nealis M, Farrell B, Mathieson JR, Penn AM. Retrospective evaluation of a clinical decision support tool for effective computed tomography angiography utilization in urgent brain imaging of suspected TIA/minor stroke in the emergency department. CJEM. 2019 May;21(3):343-351. [PubMed: 30277176]
Johnston SC, Nguyen-Huynh MN, Schwarz ME, Fuller K, Williams CE, Josephson SA, Hankey GJ, Hart RG, Levine SR, Biller J, Brown RD, Sacco RL, Kappelle LJ, Koudstaal PJ, Bogousslavsky J, Caplan LR, van Gijn J, Algra A, Rothwell PM, Adams HP, Albers GW. National Stroke Association guidelines for the management of transient ischemic attacks. Ann Neurol. 2006 Sep;60(3):301-13. [PubMed: 16912978]
Cutting S, Regan E, Lee VH, Prabhakaran S. High ABCD2 Scores and In-Hospital Interventions following Transient Ischemic Attack. Cerebrovasc Dis Extra. 2016;6(3):76-83. [PMC free article: PMC5091225] [PubMed: 27721312]
Bath PM, Woodhouse LJ, Appleton JP, Beridze M, Christensen H, Dineen RA, Flaherty K, Duley L, England TJ, Havard D, Heptinstall S, James M, Kasonde C, Krishnan K, Markus HS, Montgomery AA, Pocock S, Randall M, Ranta A, Robinson TG, Scutt P, Venables GS, Sprigg N. Triple versus guideline antiplatelet therapy to prevent recurrence after acute ischaemic stroke or transient ischaemic attack: the TARDIS RCT. Health Technol Assess. 2018 Aug;22(48):1-76. [PMC free article: PMC6139477] [PubMed: 30179153]
Boulanger JM, Lindsay MP, Gubitz G, Smith EE, Stotts G, Foley N, Bhogal S, Boyle K, Braun L, Goddard T, Heran M, Kanya-Forster N, Lang E, Lavoie P, McClelland M, O'Kelly C, Pageau P, Pettersen J, Purvis H, Shamy M, Tampieri D, vanAdel B, Verbeek R, Blacquiere D, Casaubon L, Ferguson D, Hegedus Y, Jacquin GJ, Kelly M, Kamal N, Linkewich B, Lum C, Mann B, Milot G, Newcommon N, Poirier P, Simpkin W, Snieder E, Trivedi A, Whelan R, Eustace M, Smitko E, Butcher K. Canadian Stroke Best Practice Recommendations for Acute Stroke Management: Prehospital, Emergency Department, and Acute Inpatient Stroke Care, 6th Edition, Update 2018. Int J Stroke. 2018 Dec;13(9):949-984. [PubMed: 30021503]
Ranta A, Dovey S, Gommans J, Tilyard M, Weatherall M. Impact of General Practitioner Transient Ischemic Attack Training on 90-Day Stroke Outcomes: Secondary Analysis of a Cluster Randomized Controlled Trial. J Stroke Cerebrovasc Dis. 2018 Jul;27(7):2014-2018. [PubMed: 29610038]
Rothwell PM, Giles MF, Chandratheva A, Marquardt L, Geraghty O, Redgrave JN, Lovelock CE, Binney LE, Bull LM, Cuthbertson FC, Welch SJ, Bosch S, Alexander FC, Silver LE, Gutnikov SA, Mehta Z., Early use of Existing Preventive Strategies for Stroke (EXPRESS) study. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. 2007 Oct 20;370(9596):1432-42. [PubMed: 17928046]
Hackam DG, Spence JD. Combining multiple approaches for the secondary prevention of vascular events after stroke: a quantitative modeling study. Stroke. 2007 Jun;38(6):1881-5. [PubMed: 17431209]
Wang Y, Johnston SC, Wang Y. Clopidogrel with aspirin in minor stroke or transient ischemic attack. N Engl J Med. 2013 Oct 03;369(14):1376-7. [PubMed: 24088101]
Johnston SC, Easton JD, Farrant M, Barsan W, Conwit RA, Elm JJ, Kim AS, Lindblad AS, Palesch YY., Clinical Research Collaboration, Neurological Emergencies Treatment Trials Network, and the POINT Investigators. Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA. N Engl J Med. 2018 Jul 19;379(3):215-225. [PMC free article: PMC6193486] [PubMed: 29766750]
Chimowitz MI, Lynn MJ, Derdeyn CP, Turan TN, Fiorella D, Lane BF, Janis LS, Lutsep HL, Barnwell SL, Waters MF, Hoh BL, Hourihane JM, Levy EI, Alexandrov AV, Harrigan MR, Chiu D, Klucznik RP, Clark JM, McDougall CG, Johnson MD, Pride GL, Torbey MT, Zaidat OO, Rumboldt Z, Cloft HJ., SAMMPRIS Trial Investigators. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med. 2011 Sep 15;365(11):993-1003. [PMC free article: PMC3552515] [PubMed: 21899409]
Clare CS. Role of the nurse in stroke rehabilitation. Nurs Stand. 2018 Oct 01;33(7):59-66. [PubMed: 30132306]
Basaraba JE, Picard M, George-Phillips K, Mysak T. Pharmacists as Care Providers for Stroke Patients: A Systematic Review. Can J Neurol Sci. 2018 Jan;45(1):49-55. [PubMed: 28929979]

Disclosure: Kiran Panuganti declares no relevant financial relationships with ineligible companies.

Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.

Disclosure: Forshing Lui declares no relevant financial relationships with ineligible companies.

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Bookshelf ID: NBK459143PMID: 29083778


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