Differential Diagnosis of Transient Ischemic Attack (TIA): A Comprehensive Guide for Clinicians

A transient ischemic attack (TIA), often referred to as a “mini-stroke,” is a critical medical condition demanding immediate attention. It’s characterized by a temporary disruption of blood flow to the brain, spinal cord, or retina, leading to transient neurological symptoms without causing permanent tissue damage. Recognizing and promptly evaluating a TIA is paramount as it serves as a significant warning sign for future, more severe strokes. This article delves into the Differential Diagnosis Of Tia, emphasizing the importance of distinguishing it from conditions that mimic its symptoms to ensure accurate diagnosis and timely intervention. Effective management following a TIA can dramatically reduce the risk of subsequent strokes by as much as 80%. This guide is designed to enhance clinicians’ understanding of TIA’s differential diagnosis and to refine evaluation strategies for improved patient outcomes.

Understanding the Etiology of TIA

Similar to ischemic strokes, TIAs are categorized into subtypes based on their underlying pathophysiological mechanisms. These include:

• Large Artery Atherothrombosis: This involves the formation of blood clots in large arteries, either within the skull (intracranial) or outside (extracranial). The primary mechanism is often artery-to-artery embolism, where a clot breaks off and travels to block smaller vessels downstream.
• Cardiac Embolism: Clots originating from the heart, frequently from the left atrium in patients with atrial fibrillation, can travel to the brain and cause TIAs.
• Small Vessel Disease (Lacunar Infarcts): This subtype arises from diseases affecting small arteries in the brain, such as lipohyalinosis or arteriolosclerosis, often exacerbated by hypertension, diabetes, and aging.
• Cryptogenic TIA: These TIAs lack a clear identifiable cause from large artery disease or cardiac sources. They are increasingly recognized as ESUS (embolic stroke of unknown source).
• Uncommon Etiologies: Rarer causes include arterial dissection, vasculitis, and hypercoagulable states.

Common risk factors that predispose individuals to TIA are consistent with those for stroke and cardiovascular diseases, including hypertension, diabetes mellitus, advanced age, smoking, obesity, excessive alcohol consumption, unhealthy dietary habits, psychological stress, and physical inactivity. A history of stroke or TIA significantly elevates the risk of future events. Hypertension remains the most critical modifiable risk factor both at individual and population levels.

Epidemiology of TIA

Determining the precise incidence of TIA is challenging due to the transient nature of symptoms and overlap with other conditions. However, in the United States, estimates suggest approximately half a million TIAs occur annually, with a prevalence of about 2% among adults. Notably, individuals with a prior stroke history exhibit a higher prevalence of TIA. Studies indicate that a significant proportion of stroke patients experienced TIA symptoms prior to their stroke, highlighting TIA as a crucial warning sign.

Pathophysiology of Transient Ischemic Attacks

The fundamental pathophysiology of TIA involves a temporary cessation of blood flow in a specific brain area supplied by an affected artery. The mechanisms vary by subtype:

• Large Artery Atherothrombosis: Blood flow is disrupted either due to reduced flow distal to an arterial narrowing or, more commonly, by embolization from the artery to artery.
• Small Vessel Ischemic Diseases: Conditions like lipohyalinosis or arteriolosclerosis, often linked to hypertension, diabetes, and aging, lead to small vessel obstruction.
• Cardiac Embolism: Cardiac conditions, particularly atrial fibrillation, can lead to clot formation in the heart chambers, which can then embolize to the brain.
• Cryptogenic TIA/ESUS: Characterized by cortical ischemia without identifiable large artery or cardiac embolic sources, often suggesting undetected or less common embolic mechanisms.
• Other Uncommon Causes: These encompass conditions like arterial dissection and hypercoagulable states that impair cerebral blood flow.

History and Physical Examination in TIA Assessment

Often, TIA symptoms resolve by the time a patient seeks medical attention. A detailed history is crucial, focusing on the onset, duration, and nature of neurological symptoms, including associated and relieving factors. It’s important to identify vascular risk factors such as coronary artery disease, smoking habits, substance abuse, obesity, diabetes, dyslipidemia, and hypertension, alongside personal or family histories of hypercoagulability, stroke, or TIA. Specific historical clues, such as transient monocular blindness (amaurosis fugax) described as a curtain descending, may suggest carotid artery disease. Cortical symptoms like aphasia or visual field deficits point towards a cortical TIA rather than a lacunar syndrome.

The physical examination should prioritize identifying focal neurological deficits and speech disturbances, the most common TIA presentations. Cranial nerve assessments may reveal monocular blindness, gaze palsies, facial weakness, hemianopia, diplopia, tongue or swallowing difficulties, and auditory dysfunction. Motor findings can include unilateral weakness, altered muscle tone, abnormal reflexes, and coordination issues. A thorough cardiac exam and auscultation for carotid bruits are essential. Fundoscopic examination is important to detect vascular changes from hypertension or diabetes and may reveal Hollenhorst plaques indicative of carotid artery disease.

Evaluation Strategies for TIA

The goals of TIA evaluation are multifaceted:

1. Confirm Vascular Origin: Establish that symptoms are due to vascular issues, either by detecting hypoperfusion, infarction, or identifying a potential source like arterial stenosis.
2. Rule Out Non-Ischemic Causes: Exclude conditions that mimic TIA symptoms but are not vascular in origin.
3. Determine Vascular Mechanism: Identify the specific cause (large-vessel, cardioembolic, small-vessel) to guide secondary prevention strategies.
4. Prognostic Risk Stratification: Assess the patient’s risk profile to determine appropriate management intensity and urgency.

Current guidelines emphasize neuroimaging within 24 hours of symptom onset, with MRI, particularly diffusion-weighted imaging (DWI), being preferred for its sensitivity in detecting small infarcts. CT scans, ideally CT angiography, are recommended when MRI is unavailable. Cervicocephalic vascular imaging using carotid ultrasound, transcranial Doppler, MRA, or CTA is crucial to identify treatable atherosclerotic lesions, especially in carotid arteries for potential endarterectomy within one week of symptom onset.

Cardiac evaluation should include ECG and echocardiography (transthoracic or transesophageal) to identify cardioembolic sources like atrial fibrillation, valvular disease, thrombi, or patent foramen ovale. Prolonged cardiac rhythm monitoring with Holter monitors or outpatient event recorders is advisable for cryptogenic TIAs, particularly to detect paroxysmal atrial fibrillation. Routine blood tests, including CBC, PT/INR, CMP, fasting glucose, lipid panel, and ESR, are also recommended to assess for underlying metabolic and hematologic conditions.

The ABCD2 score is a critical tool for risk stratification, predicting short-term stroke risk post-TIA based on Age, Blood pressure, Clinical features, Duration of symptoms, and Diabetes. Scores help determine the urgency of intervention and hospitalization needs, with higher scores indicating greater risk and need for immediate action.

Treatment and Management of TIA

The primary goal of TIA management is to aggressively reduce the risk of subsequent stroke. Early intervention post-TIA is crucial, as the highest stroke risk period is within the first 48 hours and the overall 3-month stroke risk can be as high as 20%. Management strategies focus on addressing the underlying etiology and implementing immediate secondary prevention measures.

Expedited evaluation and treatment, including polytherapy approaches, have been shown to significantly decrease stroke risk. Studies like EXPRESS have demonstrated up to an 80% reduction in stroke risk with early intervention. Comprehensive approaches involving diet modification, regular exercise, antiplatelet agents, statins, and antihypertensive medications can reduce subsequent vascular events by 80-90%.

Antiplatelet therapy is a cornerstone of TIA treatment. Current evidence supports dual antiplatelet therapy with aspirin and clopidogrel for a short period (3 weeks to 1 month) followed by single antiplatelet therapy. For patients with specific etiologies like significant carotid stenosis (70% or greater), revascularization procedures such as carotid endarterectomy may be indicated, although aggressive medical therapy is increasingly effective. In cardioembolic TIA, particularly due to atrial fibrillation, oral anticoagulation is the treatment of choice.

Differential Diagnosis of TIA: Mimics and Distinguishers

Accurately diagnosing TIA involves differentiating it from a range of conditions that can present with similar neurological symptoms. A thorough differential diagnosis is crucial to avoid misdiagnosis and ensure appropriate management. Key conditions to consider include:

1. Migraine with Aura

Mimicry: Migraines, especially those with aura, can cause transient neurological deficits such as visual disturbances (scotomas, flashing lights), sensory changes (numbness, tingling), and even motor weakness, mimicking TIA symptoms.

Distinguishing Features:

• Headache: Migraine auras are often followed by a headache, which is typically throbbing, unilateral, and associated with nausea, vomiting, and sensitivity to light and sound. TIA symptoms are typically not associated with headache at onset, though headache can develop later in some stroke presentations.
• Symptom Progression: Migraine aura symptoms tend to develop gradually over minutes (5-20 minutes) and can sequentially evolve (e.g., visual aura followed by sensory aura). TIA symptoms usually have a sudden onset, reaching maximal deficit within seconds to minutes.
• Duration: Migraine auras typically last longer than TIAs, often 20-60 minutes, and can extend up to an hour. While the classic definition of TIA was time-based (<1 hour), the current tissue-based definition recognizes that some TIAs can be shorter or longer. However, most TIAs resolve within minutes.
• Positive vs. Negative Symptoms: Migraine auras often involve “positive” symptoms (something being added, like flashing lights or tingling), whereas TIAs more often present with “negative” symptoms (loss of function, like weakness or vision loss). However, this is not always a reliable differentiator.
• History of Migraines: Patients with a known history of migraines, especially with aura, are more likely to be experiencing a migraine aura. However, it is crucial to remember that patients with migraine can also have TIAs, especially those with vascular risk factors.
• Neuroimaging: In cases of diagnostic uncertainty, particularly if the neurological event is atypical for migraine or if there are new neurological findings, neuroimaging (MRI with DWI) is essential to rule out TIA or stroke. Migraine auras should not cause acute infarction on DWI.

2. Seizures (Focal Seizures with Todd’s Paralysis)

Mimicry: Focal seizures can manifest with motor, sensory, visual, or language disturbances, which can be mistaken for TIA symptoms. Postictal Todd’s paralysis, a transient weakness following a seizure, can particularly mimic a TIA.

Distinguishing Features:

• Seizure Activity: Seizures are often characterized by rhythmic, jerky movements (clonic activity), muscle stiffening (tonic activity), or automatisms (unusual behaviors). However, some focal seizures may have subtle motor manifestations or primarily sensory or experiential symptoms.
• Loss of Consciousness: Generalized seizures typically involve loss of consciousness. Focal seizures may or may not impair awareness. TIA usually does not involve loss of consciousness unless there is basilar artery ischemia affecting the reticular activating system.
• Postictal State: Following a seizure, patients often experience a postictal state characterized by confusion, drowsiness, headache, and sometimes focal neurological deficits (Todd’s paralysis). This postictal state can last from minutes to hours. TIA symptoms resolve without a postictal confusional state.
• Todd’s Paralysis: This postictal weakness can mimic TIA-related weakness. However, Todd’s paralysis is directly linked to a preceding seizure and usually resolves within 24 hours.
• Electroencephalogram (EEG): EEG is helpful in distinguishing seizures from TIAs, especially if the diagnosis is unclear. An EEG performed soon after the event may show epileptiform activity in cases of seizure.
• Clinical Context: History of epilepsy or prior seizures increases the likelihood of a seizure. However, new-onset seizures in older adults, especially those with vascular risk factors, require careful evaluation to rule out stroke or TIA as a potential underlying cause.

3. Syncope and Presyncope

Mimicry: Syncope (fainting) and presyncope (near fainting) can sometimes be associated with transient neurological symptoms due to global cerebral hypoperfusion, which may be confused with TIA, especially if the syncopal episode is brief and focal neurological symptoms are present.

Distinguishing Features:

• Global Symptoms: Syncope typically involves global symptoms of cerebral hypoperfusion such as lightheadedness, dizziness, weakness, visual blurring or “graying out,” and loss of consciousness. TIA symptoms are focal, related to a specific vascular territory in the brain.
• Provoking Factors: Syncope is often provoked by triggers such as prolonged standing, dehydration, pain, emotional stress, or cardiac arrhythmias. TIAs are less likely to have such clear triggers, although posture changes can sometimes influence symptoms in patients with severe carotid stenosis.
• Loss of Consciousness: Syncope involves a loss of consciousness, albeit often brief. While TIAs do not typically cause loss of consciousness, syncope is defined by it.
• Recovery: Recovery from syncope is usually rapid and complete, without persistent focal neurological deficits. TIA symptoms, by definition, resolve, but the focus is on the focal neurological deficit itself during the event, not loss of consciousness.
• Orthostatic Blood Pressure: Measuring blood pressure in supine and standing positions can help identify orthostatic hypotension as a cause of syncope.
• Cardiac Evaluation: Given that cardiac arrhythmias can cause syncope, cardiac evaluation (ECG, Holter monitor) may be warranted, especially in older patients or those with cardiac risk factors.

4. Vertigo and Vestibular Disorders

Mimicry: Vertigo, especially acute onset vertigo, can sometimes be confused with posterior circulation TIA, as both can cause dizziness, imbalance, and other neurological symptoms.

Distinguishing Features:

• Nature of Dizziness: Vertigo is characterized by a sensation of spinning or movement of oneself or the environment. Dizziness in TIA can be less specific, but focal neurological symptoms are more indicative of TIA.
• Associated Symptoms: Vestibular disorders often present with nausea, vomiting, nystagmus, and gait unsteadiness. Posterior circulation TIAs can also cause these symptoms, along with other brainstem signs (diplopia, dysarthria, dysphagia, weakness, sensory loss).
• Nystagmus: The type of nystagmus can help differentiate peripheral vestibular vertigo (e.g., benign paroxysmal positional vertigo – BPPV, vestibular neuritis) from central vertigo (e.g., brainstem TIA). Peripheral vertigo typically has horizontal or torsional nystagmus that fatigues with repeated testing, while central vertigo can have vertical or purely torsional nystagmus and does not fatigue.
• Dix-Hallpike Test: This test is diagnostic for BPPV, a common cause of peripheral vertigo. A positive Dix-Hallpike test (eliciting vertigo and characteristic nystagmus) points towards BPPV rather than TIA.
• Focal Neurological Deficits: The presence of other focal neurological deficits (weakness, sensory loss, visual field defects, language disturbance) strongly suggests TIA, particularly posterior circulation TIA if vertigo is present. Isolated vertigo without other focal neurological signs is less likely to be TIA.
• Neuroimaging: If there is suspicion of central vertigo or posterior circulation TIA, especially with risk factors for stroke or new onset vertigo in a high-risk patient, MRI (DWI) is crucial to rule out ischemia.

5. Metabolic Disturbances (Hypoglycemia, Electrolyte Imbalances)

Mimicry: Severe hypoglycemia or electrolyte imbalances (e.g., hyponatremia, hypercalcemia) can cause a range of neurological symptoms, including confusion, weakness, seizures, and focal deficits, which could be misinterpreted as TIA.

Distinguishing Features:

• Systemic Symptoms: Metabolic disturbances often present with more generalized symptoms such as altered mental status, confusion, lethargy, or generalized weakness, rather than purely focal neurological deficits seen in TIA.
• Blood Glucose Level: Measuring blood glucose is critical, especially in patients with diabetes or altered mental status. Hypoglycemia can rapidly cause neurological symptoms that can mimic stroke or TIA.
• Electrolyte Panel: Assessing serum electrolytes (sodium, potassium, calcium) can identify imbalances that could explain neurological symptoms.
• Temporal Profile: Symptoms from metabolic disturbances may develop more gradually than the sudden onset of TIA symptoms, although hypoglycemia can also have a relatively rapid onset.
• Response to Correction: Neurological symptoms due to metabolic disturbances typically improve or resolve with correction of the underlying metabolic abnormality (e.g., glucose administration for hypoglycemia, electrolyte repletion). TIA symptoms resolve spontaneously, but not necessarily in direct response to metabolic correction.

6. Multiple Sclerosis (MS) Flare-Ups

Mimicry: MS exacerbations can cause a wide variety of neurological symptoms, including sensory loss, weakness, visual disturbances (optic neuritis, diplopia), and imbalance, which can overlap with TIA presentations, especially in younger individuals.

Distinguishing Features:

• Age of Onset: MS typically presents in younger adults (20-40 years), while TIA is more common in older individuals, although both can occur across age ranges.
• History of MS: A known history of MS makes an MS flare-up more likely. However, patients with MS can also have TIAs, especially with vascular risk factors.
• Symptom Progression: MS exacerbations often develop subacutely over days to weeks, while TIA symptoms are sudden in onset. However, some MS relapses can have a more rapid onset.
• Prior MS Symptoms: Reviewing the patient’s past neurological history for prior episodes suggestive of MS (optic neuritis, sensory symptoms, weakness) is important.
• Neurological Examination: MS may present with signs of demyelination such as optic neuritis (afferent pupillary defect, visual field loss, pain with eye movement), internuclear ophthalmoplegia, and evidence of lesions disseminated in time and space on neurological examination.
• MRI Brain and Spinal Cord: MRI is crucial for diagnosing MS and differentiating it from TIA. MS plaques are typically seen in periventricular white matter, juxtacortical regions, corpus callosum, and spinal cord. DWI in TIA shows acute ischemia, while MS plaques are chronic lesions.

7. Bell’s Palsy

Mimicry: Bell’s palsy, causing sudden onset facial weakness, can be mistaken for TIA, particularly if the patient or clinician focuses solely on the facial droop.

Distinguishing Features:

• Facial Nerve Distribution: Bell’s palsy affects the entire half of the face, including the forehead (inability to raise eyebrow, wrinkle forehead), eye (inability to close eye completely), and lower face (nasolabial fold flattening, mouth drooping). TIA-related facial weakness typically spares the forehead because of bilateral cortical innervation of the upper facial muscles.
• Associated Symptoms: Bell’s palsy can be associated with altered taste sensation, hyperacusis (increased sensitivity to sound), and ear pain on the affected side. TIA usually does not have these features related to the facial nerve itself.
• Other Neurological Deficits: Bell’s palsy is an isolated facial nerve neuropathy. The absence of other neurological deficits (weakness, sensory loss, language disturbance, visual field defects) is typical for Bell’s palsy and distinguishes it from TIA.
• Examination: Careful neurological examination to rule out other focal deficits is essential. Assess limb strength, sensation, speech, and vision to differentiate Bell’s palsy from TIA.

8. Intracranial Hemorrhage (Subarachnoid Hemorrhage, Intracerebral Hemorrhage)

Mimicry: While intracranial hemorrhage is typically more severe and persistent than TIA, some smaller hemorrhages, particularly subarachnoid hemorrhage (SAH) from a ruptured aneurysm or non-aneurysmal perimesencephalic hemorrhage, can initially present with transient or fluctuating symptoms that might be confused with TIA.

Distinguishing Features:

• Headache: SAH classically presents with a “thunderclap headache”—sudden onset, severe headache, often described as “the worst headache of my life.” While headache can occur in stroke and TIA, the severity and suddenness of SAH headache are distinctive. Intracerebral hemorrhage also often presents with headache, but may be less sudden and severe initially.
• Nuchal Rigidity: Meningeal irritation from SAH can cause nuchal rigidity (stiff neck), which is not typical for TIA.
• Altered Consciousness: Larger intracranial hemorrhages can cause rapid decline in consciousness. Smaller hemorrhages may initially have fluctuating or transient symptoms. TIA typically does not cause altered consciousness unless it is a basilar artery TIA affecting the brainstem reticular activating system.
• Neuroimaging: CT scan without contrast is highly sensitive for detecting acute intracranial hemorrhage, including SAH and intracerebral hemorrhage. It is a critical initial step in evaluating suspected TIA to rule out hemorrhage, especially if there is headache or altered consciousness. MRI (DWI) is more sensitive for detecting acute ischemia of TIA but less sensitive for acute hemorrhage than CT in the first few hours.

9. Space-Occupying Lesions (Brain Tumors, Subdural Hematoma)

Mimicry: Rarely, brain tumors or chronic subdural hematomas can present with fluctuating or progressive neurological deficits that might initially be mistaken for TIA, particularly if the symptoms are transient or fluctuating.

Distinguishing Features:

• Symptom Progression: Symptoms from space-occupying lesions tend to be progressive over days to weeks, rather than the sudden onset and resolution of TIA. However, some tumors can present acutely due to hemorrhage or seizure. Subdural hematomas can have variable presentations, sometimes with waxing and waning symptoms.
• Headache: Headache is a common symptom of brain tumors and subdural hematomas, often persistent and worsening over time, which is not typical for TIA.
• Focal Deficits: Space-occupying lesions cause focal neurological deficits based on their location, which can overlap with TIA symptoms. However, the temporal profile and progression are usually different.
• Neuroimaging: CT or MRI brain is essential to diagnose space-occupying lesions. These imaging modalities will clearly show tumors or subdural hematomas, differentiating them from the vascular territory ischemia seen in TIA (if DWI is positive) or normal imaging in TIA (if DWI is negative).

10. Drug Intoxication or Withdrawal

Mimicry: Certain drugs (e.g., stimulants, hallucinogens) and drug withdrawal syndromes (e.g., alcohol, benzodiazepine withdrawal) can cause neurological symptoms, including seizures, altered mental status, and focal deficits, which might be confused with TIA.

Distinguishing Features:

• History of Substance Use: Obtaining a history of substance use or recent cessation is crucial.
• Systemic Signs: Drug intoxication or withdrawal may present with systemic signs such as tachycardia, hypertension, diaphoresis, agitation, or tremors, depending on the substance.
• Toxicology Screen: Urine or blood toxicology screens can identify recent drug use.
• Clinical Context: The clinical context, including patient age, medical history, and circumstances surrounding the event, helps in considering drug-related causes.
• Improvement with Detoxification: Symptoms due to drug withdrawal typically improve with detoxification and supportive care. TIA requires vascular risk factor management and secondary prevention strategies.

11. Conversion Disorder (Functional Neurological Disorder)

Mimicry: Conversion disorder can present with a wide range of neurological symptoms, including weakness, sensory loss, gait disturbance, and speech problems, that can mimic TIA.

Distinguishing Features:

• Inconsistency: Symptoms in conversion disorder are often inconsistent over time or with examination, and may not follow typical neuroanatomical patterns. For example, weakness may be variable or give way on repeated testing (give-way weakness). Sensory loss may be non-anatomic (e.g., stocking-glove distribution not following dermatomes).
• Lack of Objective Findings: Neurological examination in conversion disorder may not show objective signs of neurological disease (e.g., reflexes, muscle tone, muscle bulk may be normal despite reported weakness). In TIA, neurological deficits are typically objective and consistent.
• Psychological Factors: Conversion disorder is often associated with psychological stress or underlying psychiatric conditions.
• No Vascular Risk Factors: Patients with conversion disorder may lack vascular risk factors for TIA. However, this is not a reliable differentiator as anyone can develop a functional neurological disorder.
• Clinical Course: Symptoms of conversion disorder may be more persistent or recurrent than the transient and resolving nature of TIA.
• Diagnosis of Exclusion: Conversion disorder is a diagnosis of exclusion, made after ruling out organic neurological causes, including TIA. Neuroimaging (MRI with DWI) is essential to exclude TIA or stroke before considering a functional neurological disorder.

Staging and Risk Stratification

Risk stratification scores, like the ABCD2 score, are vital for managing TIA patients. The ABCD2 score assesses stroke risk based on Age, Blood pressure, Clinical features, Duration of symptoms, and Diabetes. Scores range from 0 to 7, with higher scores indicating a greater short-term stroke risk. Patients with ABCD2 scores of 6-7 face an approximately 8% stroke risk within 48 hours, while those with scores less than 4 have about a 1% risk. These scores guide decisions regarding hospitalization and the intensity of acute management. However, it’s crucial to remember that even patients with low ABCD2 scores can have significant underlying vascular pathology, such as critical carotid stenosis, necessitating thorough evaluation.

Pearls and Key Considerations

Differentiating TIA from its mimics is critical for appropriate clinical management. Early diagnosis and treatment of TIA are essential to prevent future strokes. While the differential diagnosis of TIA is broad, a systematic approach focusing on symptom characteristics, associated features, risk factors, and targeted investigations, particularly neuroimaging, can improve diagnostic accuracy. Always consider TIA as a medical emergency requiring prompt evaluation and intervention in patients presenting with acute onset, transient neurological symptoms.

Enhancing Healthcare Team Outcomes

Effective management of TIA patients requires a collaborative interprofessional team approach. Emergency department and primary care clinicians are often the first points of contact. Nurses trained in stroke recognition are crucial for rapid triage and neurological assessment. Neurologists provide specialized expertise in diagnosis and management. Pharmacists play a key role in medication management, especially antiplatelet and anticoagulant therapies. Patient education regarding risk factor modification, medication adherence, and stroke symptom recognition is vital and involves the entire team. Improved coordination and communication among healthcare professionals are essential to optimize outcomes for patients following a TIA.