Continuing Education Activity

Transient ischemic attack (TIA) represents an acute, transient episode of focal neurologic dysfunction resulting from cerebral, spinal, or retinal ischemia without acute infarction, now defined by tissue-based criteria rather than symptom duration. This course reviews the urgent evaluation, rapid neuroimaging, vascular assessment, and etiologic classification required for this medical emergency and major predictor of impending ischemic stroke. This activity outlines the differentiation of TIA from mimics while identifying mechanisms such as large-artery atherothrombosis, cardioembolism, or small-vessel disease. Participants will gain an understanding of early recognition, risk stratification, clinical tools such as the ABCD2 score, interpretation of neurovascular imaging, and initiation of evidence-based secondary prevention strategies, including antiplatelet therapy, statins, blood pressure control, and targeted management of underlying causes. This activity for healthcare professionals is designed to enhance the learner's competence in identifying TIA, performing the recommended time-sensitive evaluation, and implementing an appropriate interprofessional approach when managing this condition to improve long-term neurologic outcomes.

Objectives:

• Differentiate transient ischemic attack from common mimicking conditions based on diagnostic findings.
• Assess stroke risk using clinical red-flag features to determine the need for expedited intervention.
• Implement guideline-directed secondary prevention strategies within the acute posttransient ischemic attack period.
• Collaborate with interprofessional team members to improve care coordination and improve outcomes in patients who have had a transient ischemic attack.

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Introduction

Transient ischemic attack (TIA) constitutes a medical emergency characterized by an acute, transient episode of focal neurologic dysfunction within a vascular territory resulting from ischemia of the brain, spinal cord, or retina, with complete resolution of symptoms and no evidence of acute infarction or tissue injury. The definition of TIA has evolved from a time-based framework to a tissue-based framework. Symptom duration generally lasts less than 1 hour, more commonly only a few minutes. TIA serves as a significant warning sign of an impending ischemic stroke, with the highest risk occurring during the first 48 hours after the event.[1]

Accurate differentiation of TIA from conditions that mimic cerebrovascular ischemia remains essential for appropriate management. TIAs commonly present with focal neurologic deficits and/or speech disturbances localized to a vascular territory and associated with underlying cerebrovascular disease. Symptom onset occurs abruptly and reaches maximal intensity at presentation. Urgent evaluation with appropriate imaging and laboratory studies supports diagnosis and helps reduce the risk of subsequent stroke. Clinical risk stratification tools assist in estimating the likelihood of recurrent TIA or ischemic stroke and guide management decisions.

Immediate implementation of multimodal therapeutic interventions remains critical following diagnosis. Recommended measures include aggressive blood pressure management, high-dose statin therapy, antiplatelet treatment, glycemic control, dietary modification, and regular physical activity. Management should also target the specific underlying etiology responsible for the ischemic event. This comprehensive treatment strategy may reduce the risk of recurrent stroke or future TIA by at least 80%.[2][3][4][5][6]

Etiology

TIA subtypes, classified according to the pathophysiological mechanisms, are similar to ischemic stroke subtypes. These underlying causes include large-artery atherothrombosis, cardiac embolism, small-vessel (lacunar), cryptogenic, and uncommon subtypes, eg, vascular dissection and vasculitis. 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 substantially increase the subsequent risk of recurrent stroke or TIA.[7][8] Among all risk factors, hypertension is the most important for an individual and for a population.

Epidemiology

Accurate estimation of TIA incidence within the general population remains challenging because numerous neurologic and non-neurologic conditions can mimic its clinical presentation. Despite these diagnostic challenges, at least 240,000 individuals experience a TIA each year in the United States.[5]

The estimated overall prevalence of TIA among adults in the United States approaches 2%. Research has demonstrated a higher prevalence of TIA among individuals with a prior history of stroke. Several studies have also reported that a substantial proportion of patients presenting with an initial ischemic stroke experienced preceding TIA symptoms, highlighting the role of TIA as an important warning event that often precedes a more severe cerebrovascular outcome.[7]

Pathophysiology

The most common underlying pathophysiological mechanism of TIA is the transient interruption of arterial blood flow to an area of the brain supplied by a specific artery. According to the TOAST classification of stroke, the pathophysiology of TIA varies by subtype as follows:

• Large-artery atherothrombosis: This may be intracranial or extracranial. The mechanism may be a lack of blood flow distal to the site of arterial stenosis or an artery-to-artery embolism, the latter of which is more common.
• 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 ischemic pattern without any identifiable large-artery atherothrombosis or a cardiac source of emboli. More recently, it is often referred to as ESUS (embolic stroke of unknown source).
• Other uncommon causes (eg, arterial dissection or hypercoagulable states) [9][10]

History and Physical

Clinical History

TIA symptoms are typically abrupt in onset, with maximal deficit at the time of onset. The symptoms often resolve by the time the patient presents to her doctor or emergency department. The duration is most often minutes, rarely over an hour. 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, including 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, eg, 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, eg, language disturbance or visual field loss, will point to a cortical TIA rather than a lacunar syndrome.[5] Please see StatPearls' companion resource, "Lacunar Stroke," for further information on lacunar syndromes.

Physical Examination

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 may reveal monocular blindness, disconjugate gaze, facial droop, hemianopia, diplopia, abnormal tongue movement, difficulty swallowing, and auditory dysfunction. Some of the motor findings include unilateral weakness of the upper or lower extremities, face, and tongue; increased tone; clonus; rigidity; and abnormal reflexes, which may occur with TIA. Cardiac examination and carotid auscultation for a carotid bruit are very important. Fundoscopy is important for detecting fundoscopic evidence of vascular changes resulting from hypertension or diabetes. Fundoscopy may also show a Hollenhorst plaque, which will indicate an underlying internal carotid artery disease. Please see StatPearls' companion resource, "Hollenhorst Plaque," for further information.

The clinical evaluation, in addition to establishing the diagnosis of TIA rather than a mimic, also yields the important ABCD2 score for subsequent stroke risk stratification. (Please refer to the Evaluation section for more information.)

Evaluation

The goals of the evaluation of TIA primarily include:

1. To prove the vascular origin of the symptoms either directly or indirectly (This means finding evidence of hypoperfusion or acute infarction, or identifying a presumptive source, eg, a large-vessel stenosis.) [5]
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

Imaging Studies

A scientific statement from the American Heart Association in 2023 recommended an initial noncontrast head computed tomography (CT) scan, followed by a multimodal brain magnetic resonance imaging (MRI), within 24 hours of symptom onset.[5] Brain MRI with diffusion-weighted imaging (DWI) within 24 hours is the preferred imaging modality given its higher sensitivity than CT in identifying small infarcts. CT and CT angiography (CTA) and perfusion (CTP) can be used if DWI MRI is contraindicated or unavailable. CTP can detect ischemic penumbra, a surrogate for DWI MRI.

Vascular imaging with ultrasonography or CTA/MRA needs to be performed urgently as part of a TIA evaluation. Carotid duplex is a good screening tool, yet CTA/MRA is needed to confirm arterial stenosis greater than 50%. CTA is performed from the aortic arch to the vertex. MRA can be performed at the same time as MR brain imaging.[11]

Additional Diagnostic Studies

Serum laboratory studies include a complete blood count (CBC), erythrocyte sedimentation rate, and coagulation studies. Other important blood tests include a complete metabolic panel, lipid panel, fasting glucose, and HbA1c. A urine drug screen may be indicated in selected cases.

Cardiac assessment should include an electrocardiogram (ECG) and transthoracic echocardiogram (TTE)/transesophageal echocardiogram (TEE) to identify a cardioembolic source and evaluate for patent foramen ovale, valvular disease, cardiac thrombus, and atherosclerosis. A Holter monitor or a 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.[12][13][8]

Stroke Risk Stratification

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

• Age older than 60 years (1 point)
• Blood pressure greater than or equal to 140/90 mm Hg on first evaluation (1 point)
• Clinical symptoms of 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 scores of 2 or 3, 4.1% for scores of 4 or 5, and 8.1% for scores of 6 or 7. Most stroke centers will admit patients with a TIA score of 4, 5, or higher for expedited management and observation. For patients with a lower score, expedited evaluation and management are still warranted. This expedited approach has been proven to improve the outcome.[14] 

Several limitations affect the predictive accuracy of the ABCD2 score. The scoring system does not account for posterior circulation TIA manifestations, including ataxia and visual field deficits. In addition, high-risk pathophysiologic mechanisms such as ipsilateral large-artery stenosis, cervical artery dissection, and atrial fibrillation fall outside the parameters included in the score. Acute vascular imaging performed during the emergency department evaluation plays a critical role in guiding immediate management decisions and identifying these high-risk features.

More recent risk stratification models incorporate imaging findings and clinical factors beyond those included in the ABCD2 score. These enhanced tools include imaging evidence, a history of 2 or more TIA episodes within the preceding 7 days, and the presence of new or prior infarctions identified on CT or MRI. Integration of these variables resulted in the development of the ABCD3-I score, which may provide more accurate risk stratification. Despite these advances, the ABCD2 score remains the most widely utilized clinical tool for assessing stroke risk after TIA.

The following are high-risk features of a TIA, and patients should be admitted to the hospital for acute management. Patients may receive expedited emergency department evaluation without these features:

• ABCD2 ≥4
• Subacute/acute infarct on CT or MRI
• ≥50% stenosis of the ipsilateral carotid stenosis
• Recent TIA in the last month
• Acute cardiac process or arrhythmia
• Other conditions requiring admission [5] 

Treatment / Management

The main aim of the 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 a TIA is extremely important. This will significantly reduce future strokes. Management of TIAs should focus on treating underlying etiologies.[15][16][17]

Studies in the new millennium have already confirmed the importance of expedited evaluation and treatment, plus the polytherapy approach. The EXPRESS study in the United Kingdom has shown the importance of early intervention over regular treatment, reducing stroke risk by 80%.[18] Hackam et al. conducted a meta-analysis in 2007 showing that a combination of diet, exercise, antiplatelet, statin, and antihypertensive therapy may reduce the risk of subsequent stroke by 80% to 90%.[19]

More recent studies in China, The Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events (CHANCE) trial, and the multinational Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke (POINT) trial also confirmed that dual antiplatelet therapy with aspirin and clopidogrel, initiated within 24 hours, for 3 weeks to 1 month, followed by a single antiplatelet agent, is the best scheme for antiplatelet therapy.[20][21] The dual antiplatelet therapy consists of low-dose aspirin (<325 mg) and clopidogrel 75 mg per day. Clopidogrel blocks platelet aggregation via the P2Y12 Receptor pathway, a mechanism that is synergistic with aspirin in platelet-aggregation assays. This is the rationale for the combination. However, clopidogrel requires the cytochrome P450 (CYP) enzyme CYP2C19 to be converted to its active form. Many patients carry a loss-of-function variant in the gene, particularly among Central and South Asians, resulting in reduced clopidogrel efficacy.[22]

Ticagrelor, another antiplatelet agent, also works through the P2Y12 receptor pathway. Ticagrelor is an active drug on its own and therefore will not be affected by any genetic enzyme issues. This agent is a logical choice for patients with a clopidogrel CYP2C19 loss-of-function variant. The THALES trial confirmed the efficacy of ticagrelor.

The following are recent important trials for secondary stroke prevention after a TIA or stroke:

• The Ticagrelor or Clopidogrel with Aspirin in High-Risk Patients with Acute Nondisabling Cerebrovascular Events II (CHANCE-2) trial: Many patients, especially among Asians, carry the clopidogrel CYP2C19 loss-of-function variant. These patients may not respond well to clopidogrel. The CHANCE-2 trial demonstrated greater efficacy at 1 year with tecagrelor-aspirin compared with clopidogrel-aspirin when initiated within 24 hours and continued for 21 days.[23]

• The Acute Stroke or Transient Ischaemic Attack Treated with Ticagrelor and ASA for Prevention of Stroke and Death (THALES) trial: the risk of stroke or death within 30 days was lower with ticagrelor–aspirin than with aspirin alone.[24]

• Clopidogrel and Aspirin Initiated between 24 and 72 Hours for Mild Ischemic Stroke (INSPIRE) trial: the efficacy of clopidogrel and aspirin initiated between 24 and 72 hours is similar to that initiated within 24 hours, yet with increased bleeding.[25]

• OCEANIC-STROKE trial: Asundexian is an inhibitor of activated clotting factor XI (FXIA). Asundexian treatment lowers the risks of ischemic stroke and major cardiovascular events compared with placebo, without a higher risk of major bleeding, in patients with noncardioembolic ischemic stroke or high-risk TIA treated with antiplatelet therapy.[26] Since asundexian is an anticoagulant with minimal bleeding issues, the agent may be a great choice for secondary prevention of cryptogenic stroke or ESUS. Clinicians should expect to see a wider use of FXIA inhibitors in the near future.

• Endovascular treatment (EVT) for medium or distal vessel occlusion stroke (DISTAL) trial: For patients with a medium or distal intracranial vessel occlusion stroke, EVT plus best medical treatment did not result in better outcomes for disability or death at 90 days or 12 months compared with best medical treatment alone.[27][28]

Management beyond initial medical therapy depends on the underlying etiology of the transient ischemic attack. Revascularization remains recommended for patients with symptomatic cervical internal carotid artery stenosis of 70% or greater. Among available revascularization strategies, carotid endarterectomy may provide a slightly more favorable benefit-to-risk profile than endovascular intervention and carotid artery stenting. Decisions regarding intervention for patients with 50% to 69% carotid stenosis require careful consideration of the surgeon’s complication rates and procedural expertise, particularly in light of the substantial advances achieved with aggressive contemporary medical therapy.

Evidence from the SAMMPRIS trial demonstrated that endovascular treatment with Wingspan stenting for 70% to 99% stenosis of major intracranial arteries offers no advantage over aggressive medical therapy alone.[29] Consequently, optimal medical management remains a cornerstone of treatment for many patients with intracranial atherosclerotic disease. For patients with atrial fibrillation or other identified cardioembolic sources of TIA, oral anticoagulation serves as the recommended strategy for secondary stroke prevention and reduction of future thromboembolic events.

Differential Diagnosis

The differential diagnoses of TIA are the TIA or stroke mimics. Please see StatPearls' companion resource, "Stroke Mimics," for further information. Mimics account for almost half of hospital admissions for suspected stroke.[30] The most common and important ones are migraine with aura and seizures. Patients suffering from TIA mimics are younger and without vascular risk factors. The symptoms may spread or march rather than be maximal at the onset. More commonly, altered mentation is present, with positive signs and symptoms of tingling, visual obscurations, and seizure-like activity. The symptoms may not be in a specific vascular territory. The stroke mimics include:

• Migraine with aura
• Epilepsy
• Meningitis
• Encephalitis
• Multiple sclerosis
• Syncope
• Peripheral vertigo
• Functional neurological disorders
• Posterior reversible vasoconstriction syndrome (PRVS)
• Transient global amnesia
• Hypoglycemia and other acute metabolic encephalopathies [31]

Staging

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 = Systolic blood pressure >140 or diastolic blood pressure >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 to 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. Although scales are important for evaluating TIA, clinicians should be aware that patients with critical carotid artery stenosis may sometimes present with a very low ABCD2 score.

Prognosis

The prognosis following a TIA depends largely on the underlying etiology, the presence of vascular risk factors, and the timeliness of diagnostic evaluation and secondary prevention. Although neurologic symptoms resolve completely, TIA should not be considered a benign event because it represents a marker of active cerebrovascular disease and a substantial risk of future ischemic stroke. The risk of stroke is highest during the first hours to days after the event, particularly within the first 48 hours. Contemporary data indicate that the risk of ischemic stroke is approximately 5% within 90 days and 5.9% within 1 year following a TIA or minor stroke. Long-term risk remains significant, with cumulative stroke rates increasing to approximately 12.8% at 5 years and nearly 19.8% at 10 years.[32] Furthermore, nearly 1 in 5 patients will experience a subsequent stroke, myocardial infarction, or death within the first year, underscoring the systemic vascular implications of TIA.[32]

Long-term outcomes are strongly influenced by aggressive risk-factor modification and adherence to evidence-based secondary prevention strategies. Patients who undergo rapid evaluation and receive appropriate interventions, including antiplatelet or anticoagulant therapy when indicated, statin treatment, blood pressure control, diabetes management, smoking cessation, dietary modification, and regular physical activity, experience substantially lower rates of recurrent cerebrovascular events. Mortality risk is greatest during the first year after a TIA and declines over time, although subsequent strokes remain associated with significant morbidity and mortality. Frailty, advanced age, uncontrolled vascular risk factors, symptomatic carotid disease, and cardioembolic conditions such as atrial fibrillation are associated with poorer outcomes and reduced life expectancy.[33] Consequently, prompt diagnosis, comprehensive etiologic evaluation, and sustained preventive care remain essential for improving prognosis and reducing the long-term burden of stroke and cardiovascular disease.

Complications

The most significant complication of a TIA is the development of an ischemic stroke. Although TIA symptoms resolve completely, the event serves as a warning sign of ongoing cerebrovascular disease and a markedly increased risk of subsequent stroke. The risk is greatest during the first 48 hours following a TIA, and approximately 20% of patients may experience a stroke within 3 months if appropriate evaluation and treatment are not initiated. Recurrent TIAs may also occur, indicating persistent vascular pathology and further elevating the risk of permanent neurologic injury. Patients with untreated carotid artery stenosis, atrial fibrillation, intracranial atherosclerosis, or poorly controlled vascular risk factors face particularly high rates of recurrent cerebrovascular events.

Additional complications arise from delayed diagnosis, failure to identify the underlying etiology, or inadequate implementation of secondary prevention strategies. Missed opportunities to initiate antiplatelet therapy, anticoagulation for cardioembolic sources, lipid-lowering treatment, or aggressive blood pressure management can lead to preventable stroke, long-term disability, cognitive impairment, reduced quality of life, and increased mortality. Recurrent cerebrovascular events may also result in prolonged hospitalization, functional dependence, and substantial healthcare utilization. Prompt recognition of TIA, comprehensive diagnostic evaluation, and timely initiation of evidence-based interventions remain essential for minimizing complications and improving long-term neurologic outcomes.

Deterrence and Patient Education

TIA prevention focuses on aggressive modification of vascular risk factors and prompt treatment of underlying etiologies. Hypertension remains the most important modifiable risk factor, making regular blood pressure monitoring and adherence to antihypertensive therapy essential components of stroke prevention. Additional preventive strategies include optimal control of diabetes mellitus and dyslipidemia, smoking cessation, moderation of alcohol consumption, maintenance of a healthy weight, regular physical activity, and adoption of a heart-healthy diet. Identification and treatment of specific causes, eg, atrial fibrillation, carotid artery stenosis, hypercoagulable states, or other cardioembolic sources, are critical for reducing the risk of recurrent TIA and ischemic stroke. Evidence demonstrates that comprehensive secondary prevention measures, including antiplatelet therapy, statin treatment, lifestyle modification, and risk-factor management, can reduce the risk of future cerebrovascular events by as much as 80% to 90%.

Patient education should emphasize that a TIA is a medical emergency rather than a benign, self-limited event. Patients and caregivers should understand that symptoms, eg, sudden unilateral weakness, facial droop, speech difficulty, vision loss, sensory changes, dizziness, or gait instability, require immediate emergency evaluation, even when symptoms resolve completely. Education should reinforce the concept that the highest risk of stroke occurs within the first 48 hours after a TIA and that delaying medical attention can result in preventable disability or death. Clinicians should encourage patients to recognize stroke warning signs and activate emergency medical services rather than attempting self-transport or waiting for symptoms to recur.

Ongoing patient counseling should focus on medication adherence, attendance at follow-up appointments, and participation in recommended diagnostic testing and monitoring. Patients prescribed antiplatelet agents, anticoagulants, statins, or antihypertensive medications should receive clear instructions regarding the purpose of each therapy and the consequences of nonadherence. Shared decision-making can help patients understand their individual stroke risk and engage actively in preventive strategies. Education involving family members and caregivers further supports recognition of recurrent symptoms, reinforces lifestyle modifications, and promotes timely communication with healthcare professionals, ultimately improving long-term outcomes and reducing the likelihood of recurrent cerebrovascular events.

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 or TIA-mimics includes but is not limited to vertigo, dizziness, seizures, headaches, Bell palsy, drug withdrawal, dementia, electrolyte disorders, acute infections, syncope, and alcoholism. Once a diagnosis of TIA is suspected, an emergent workup is indicated at the ED, including lab tests, brain imaging, and vascular imaging, and initiation of therapies to prevent subsequent TIA or strokes. All these measures should be initiated within the first 24 hours of presentation if at all possible. 

Enhancing Healthcare Team Outcomes

TIA is a neurologic emergency characterized by transient focal neurologic dysfunction caused by cerebral, spinal, or retinal ischemia without evidence of acute infarction. The tissue-based definition reflects advances in neuroimaging and emphasizes the absence of permanent tissue injury rather than symptom duration alone. Symptoms typically begin suddenly and may include unilateral weakness, speech impairment, visual disturbances, or other focal deficits corresponding to a vascular territory. Because the risk of ischemic stroke is highest within the first 48 hours after a TIA, urgent evaluation is essential and includes brain imaging, vascular imaging, cardiac assessment, laboratory studies, and risk stratification using tools such as the ABCD2 score. Management focuses on rapid identification of the underlying mechanism, initiation of antiplatelet therapy, statin treatment, blood pressure and glucose control, lifestyle modification, and treatment of specific etiologies such as carotid stenosis or atrial fibrillation to reduce recurrent cerebrovascular events.

Interprofessional collaboration is critical for optimizing outcomes and preventing subsequent stroke following TIA. Emergency physicians, neurologists, and advanced practice clinicians coordinate rapid diagnosis, risk stratification, and implementation of evidence-based treatment pathways. Primary care clinicians oversee long-term management of vascular risk factors, monitor adherence to preventive therapies, and facilitate ongoing surveillance for recurrent symptoms. Nurses perform neurologic assessments, monitor clinical status, reinforce patient education, and ensure effective communication during care transitions. Pharmacists support medication selection, evaluate potential drug interactions, promote adherence, and counsel patients regarding antiplatelet, anticoagulant, and lipid-lowering therapies. Radiologists and cardiologists contribute to the timely identification of vascular and cardioembolic sources through advanced imaging and cardiac monitoring. Shared decision-making among healthcare professionals, patients, and caregivers promotes adherence to treatment plans, timely referral for specialized interventions, and coordinated follow-up. This systems-based approach improves patient safety, reduces treatment delays, minimizes preventable complications, and supports sustained risk reduction through comprehensive secondary stroke prevention.[34][35] 

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

Disclosure: Elsa Vadakekut declares no relevant financial relationships with ineligible companies.