eMedicine Specialties > Emergency Medicine > Neurology

Transient Ischemic Attack

Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor, Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital

Updated: Nov 17, 2009

Introduction

Background

A transient ischemic attack (TIA) is considered an acute episode of temporary neurologic dysfunction caused by a vascular occlusion. Symptoms typically last less than an hour. While the classical definition included symptoms lasting as long as 24 hours, advents in neuroimaging have suggested that many such cases represent minor strokes with resolved symptoms rather than true TIAs. Current guidelines recommend that a transient ischemic attack be defined as a transient episode of neurological dysfunction caused by focal brain, spinal-cord, or retinal ischemia, without acute infarction.¹

For additional information, see Medscape's Stroke/Cerebrovascular Disease Resource Center.

Pathophysiology

Temporary reduction or cessation of cerebral blood flow in a specific neurovascular distribution can be due to low flow through a partially occluded vessel or to an acute thromboembolic event.

Frequency

United States

Between 200,000-500,000 TIAs per year are diagnosed in the United States.^2,3 ED visits for TIA occur at about 1.1 visits per 1,000 US population, and TIAs are diagnosed in 0.3% of ED visits.⁴ TIA carries a particularly high short-term risk of stroke, and approximately 15% of diagnosed strokes are preceded by TIAs.

International

TIA occurs in about 150,000 patients per year in the United Kingdom.⁵ The population incidence likely mirrors that of stroke.

Mortality/Morbidity

The most important short-term risk from a TIA is that of stroke.⁶ The early risk of stroke following TIA is approximately 4-5% at 2 days and as high as 11% at 7 days.^5,7 Additionally, despite a public education program, many patients still do not seek medical attention after experiencing TIA symptoms. Public health professionals and physicians need to do more such as promoting and participating in medical screening fairs and public outreach programs.

Race

The incidence of TIAs in blacks, at 98 cases per 100,000 population, is higher than that in whites, 81 cases per 100,000 population. Controversy exists regarding whether race influences emergent workup following TIA.^8,9

Sex

The incidence of TIAs in men, at 101 cases per 100,000, is significantly higher than that in women, 70 cases per 100,000.¹⁰

Age

The incidence of TIAs appears to increase with age, from 1-3 cases per 100,000 in those younger than 35 years to up to 1500 cases per 100,000 in those older than 85.¹¹ Fewer than 3% of all major cerebral infarcts occur in children. Pediatric strokes can often have quite different etiologies compared with adult strokes and are relatively more infrequent.

Clinical

History

A transient ischemic attack (TIA) may last only minutes and has often resolved before the patient presents to a clinician. Thus, historical questions should be addressed not just to the patient but also to family members, witnesses, and emergency medical services (EMS) personnel. Witnesses may have perceived abnormalities that the patient could not, such as changes in behavior, speech, gait, memory, and movement.

• Significant medical history questions include the following:
  • Recent surgery (eg, carotid, cardiac)
  • Previous strokes
  • Known cardiovascular disease
  • Seizures
  • CNS infections
  • Use of illicit drugs
  • Complete medication regimen
  • Comorbidities related to metabolic disorders
• Carefully investigate onset, duration, fluctuation, and intensity of symptoms.
• Reviewing the patient's medical record is extremely important for identifying deficits from previous strokes, seizures, or cardiac events. The primary care physician may have great insight into previous episodes and workup.
  • Attempt to clarify when symptoms first occurred, how long they lasted, if the patient recovered completely (returned to baseline status), and if a pattern of escalating symptoms is present. For those who woke up or are found with symptoms, the time last known to be normal should be documented.
  • History of associated trauma or cardiac symptoms widens the differential diagnosis. Pertinent negative items (eg, headache, chest pain, eye pain) in the review of systems also are important.
  • Carotid or vertebral dissection can occur in association with both major and minor trauma. The patient may provide a history of blunt or torsion injury to the neck. Controversy exists regarding whether manipulation by a chiropractor or massage therapy increases the risk of arterial dissection.¹²
• Elicit any risk factors for relevant underlying disease.
  • Known coagulopathy
  • History of arteritis
  • Noninfectious necrotizing vasculitis, drugs, irradiation, and local trauma are known to cause inflammatory arterial injury.
  • Thromboembolic risk factors such as carotid artery stenosis, venous or arterial thromboembolism, patent foramen ovale, atrial fibrillation, prior myocardial infarction, or left ventricular dysfunction.

Physical

The goal of the physical examination is to carefully uncover any neurologic deficits, evaluate for underlying cardiovascular risk factors, and seek any potential thrombotic or embolic source of the event.

Ideally, any neurologic deficits should be recorded with the aid of a formal and reproducible stroke scale, such as the National Institutes of Health Stroke Scale (NIHSS). A stroke scale prompts the examiner to be thorough and allows different examiners to reliably repeat the examination during subsequent phases of the evaluation. Any neurologic abnormalities should suggest the diagnosis of stroke (or ongoing neurologic event) rather than TIA.

• Initial vital signs should include the following:
  • Temperature
  • Blood pressure
  • Heart rate and rhythm
  • Respiratory rate and pattern
  • Oxygen saturation
• The examiner should assess the patient's overall health and appearance, making an assessment of the following:
  • Attentiveness
  • Ability to interact with the examiner
  • Language and memory skills
  • Overall hydration status
  • Development
• Identify signs of other active comorbidities including infections (eg, sinusitis, mastoiditis, meningitis) and vasculidities. Carotid arteries can be examined for pulse upstroke, bruit, and the presence of carotid endarterectomy scars.
• Funduscopy can identify retinal plaques, retinal pigmentation, and optic disc margins.
• Pupil reaction to direct and consensual light exposure can be assessed.
• In addition to performing standard auscultation, examine the chest for the presence of surgical scars or presence of a pacemaker/automatic implantable cardioverter defibrillator (AICD), or other clues that the patient may have a cardiac disorder and increased risk of a cardioembolic phenomenon.
• Cardioembolic events are significant causes of TIAs. Identify the rhythm for irregularity or other unusual rhythms and rates, murmurs, or rubs that might suggest valvular disease, atrioseptal defects, or ventricular aneurysm (a source of mural thrombi).
• A neurologic examination is the foundation of the TIA evaluation and should particularly focus on the neurovascular distribution suggested by the patient’s symptoms. Subsets of the neurologic examination include the following:
  • Cranial nerve testing
  • Somatic motor strength
  • Somatic sensory testing
  • Cerebellar system (be sure to see the patient walk)
• Mental status can be assessed formally (Mini-Mental Status Examination, Quick Confusion Scale) or as part of the patient's overall response to questions and interactions with the examiner. The following signs may be present with cranial nerve dysfunction:
  • Ocular dysmotility
  • Forehead wrinkling asymmetry
  • Incomplete eyelid closure
  • Asymmetrical mouth retraction
  • Loss of the nasolabial crease
  • Swallowing difficulty
  • Lateral tongue movement
  • Weak shoulder shrugging
  • Visual field deficits
• Somatic motor testing
  • Test muscle stretch reflexes of biceps, triceps, and brachioradialis and patellar and Achilles reflexes.
  • Inspect posture and presence of tremors. Test shoulder girdle, upper extremity, abdominal muscle, and lower extremity strength.
  • Test passive movement of major joints to look for spasticity, clonus, and rigidity.
• The cerebellar system can be tested by assessing ocular movement, gait, and finger-to-nose and heel-to-knee movements, looking for signs of past-pointing and dystaxia, hypotonia, overshooting, gait dystaxia, and nystagmus.

Causes

The transient ischemic attack (TIA) workup is focused on emergent/urgent risk stratification. A number of potential underlying causes can be rapidly identified.

• Atherosclerosis of carotid and vertebral arteries 
• Embolic sources - Valvular disease, ventricular thrombus, and thrombus formation due to atrial fibrillation
• Arterial dissection
• Arteritis - Inflammation of the arteries occurring primarily in elderly persons, especially women
  • Noninfectious necrotizing vasculitis (primary cause)
  • Drugs
  • Irradiation
  • Local trauma
• Sympathomimetic drugs (eg, cocaine)
• Mass lesions (eg, tumors, subdural hematomas) - Less frequently cause transient symptoms and more often result in progressive persistent symptoms
• TIA etiologies in children, which can be different than those in adults, include the following:
  • Congenital heart disease with cerebral thromboembolism (most common)
  • Drug abuse (eg, cocaine)
  • Clotting disorders
  • CNS infection
  • Neurofibromatosis
  • Vasculitis
  • Idiopathic progressive arteriopathy of childhood (moyamoya)
  • Fibromuscular dysplasia
  • Marfan disease
  • Tuberous sclerosis
  • Tumor

Differential Diagnoses

Workup

Laboratory Studies

• Ruling out metabolic or drug-induced etiologies for symptoms consistent with a TIA is important. Most importantly, a fingerstick blood glucose should be checked for hypoglycemia. Serum electrolytes should be sent to investigate for electrolyte derangements.
• Emergency presentation
  • Serum chemistry profile including creatinine
  • Coagulation studies
  • Complete blood count
• Typically helpful and can often be performed urgently
  • Erythrocyte sedimentation rate (ESR)
  • Cardiac enzymes
  • Lipid profile
  • Screening for hypercoagulable states (particularly in younger patients with no known vascular risk factors:¹
    • Protein C, protein S, antithrombin III activities
    • Activated protein C resistance/factor V Leiden
    • Fibrinogen
    • D-Dimer
    • Anticardiolipin antibody
    • Lupus anticoagulant
    • Homocysteine
    • Prothrombin gene G20210A mutation
    • Factor VIII
    • Von Willebrand factor
    • Plasminogen activator inhibitor-1
    • Endogenous tissue plasminogen activator activity
• As needed based upon history
  • Syphilis serology
  • Antiphospholipid antibodies
  • Toxicology screens
  • Hemoglobin electrophoresis
  • Serum protein electrophoresis
  • Cerebrospinal fluid examination

Imaging Studies

National recommendations for urgent evaluation of the patient with a transient ischemic attack (TIA) include imaging of the brain within 24 hours of symptom onset; preferably MRI with DWI, but if this is not available, then a CT scan should be obtained.^1,13 The cerebral vasculature should be imaged urgently, preferably at the same time as the brain. Brain imaging can identify an area of ischemia in up to 25% of patients, and TIA mimics may be identified as well. Vessel imaging can identify a stenosis or occlusion that requires early intervention.

• Brain imaging
  • Noncontrast cranial CT scan: This test is widely and rapidly available and often serves as the initial imaging evaluation. It can aid in diagnosing the following: 
    • A new area of ischemia or infarction
    • Old areas of ischemia
    • Intracranial mass such as tumor
    • Intracranial bleeding such as subdural hematoma or intracerebral hemorrhage 
  • MRI 
    • MRI is more sensitive for acute ischemia, infarction, previous intracranial bleeding, and other underlying lesions than CT. 
    • The presence of ischemic lesions on MRI appears to increase the short-term risk of stroke, highlighting its potential value in acute risk stratification.^14,15 In addition, a negative DWI image in concert with low-risk clinical features can mark those at minimal short-term stroke risk.¹⁶  
    • However, this study is less widely available on an acute basis than CT scan.
• Vascular imaging 
  • Carotid Doppler ultrasonography of the neck can identify patients in need of urgent surgical or endovascular therapy.
  • Transcranial Doppler can be a complementary examination evaluating patency of cerebral vessels and collateral circulation.
  • Computed tomographic angiography (CTA) is of increasing value in identifying occlusive disease in the cerebrovascular circulation.
  • Magnetic resonance angiography (MRA) is another alternative for imaging vessels in both the brain and neck.
  • Conventional angiography can be performed when the above modalities are unavailable or yield discordant results.
• Cardiac imaging: Transthoracic or transesophageal echocardiography (TTE/TEE) can evaluate for a cardioembolic source or for risk factors such as patent foramen ovale.

Other Tests

• 12-Lead electrocardiography should be performed as soon as possible after transient ischemic attack (TIA), and can evaluate for dysrhythmias such as atrial fibrillation.
• Cardiac monitoring (inpatient telemetry or Holter monitor) is recommended as "useful" in patients without a clear diagnosis after initial brain imaging and electrocardiography.
• Lumbar puncture (LP) may be indicated if subarachnoid hemorrhage, infectious etiology, or demyelinating disease is to be excluded.
• Electroencephalography (EEG) may be indicated to evaluate for seizure activity.

Treatment

Prehospital Care

• Rapid transport is essential to evaluate the patient who may have fleeting or stuttering symptoms.
• Fingerstick glucose can quickly rule out hypoglycemia.
• Intravenous (IV) access can be established, although transport should not be delayed for this.
• Collect all the patient’s prescription bottles.
• The family or witnesses should be instructed to go to the ED, or contact information for these individuals should be obtained.
• Some communities may have EMS preferentially transfer patients with high-risk stroke symptoms to centers with specific stroke expertise.¹⁷

Emergency Department Care

• Global CNS depression and airway or cardiac compromise are not typically features of a TIA. In fact, the level of consciousness and neurologic examination are expected to be at the patient's baseline.
  • Initial assessment is aimed at excluding emergent conditions that can mimic a TIA such as hypoglycemia, seizure, or intracranial hemorrhage.
  • Vital signs must be obtained promptly and addressed as indicated.
  • Cardiac monitoring can capture a relevant dysrhythmia.
  • Pulse oximetry can evaluate for hypoxia.
  • Intravenous access (if not already established by EMS) should be obtained.
  • Obtain a fingerstick glucose level and treat accordingly.
  • Laboratory studies, including CBC, coagulation studies, and electrolyte levels, should be obtained.
  • Obtain an ECG and evaluate for symptomatic rhythms or evidence of ischemia.
  • Patients may be significantly hypertensive. Unless there is specific concern for end-organ damage from a hypertensive emergency, blood pressure should be managed conservatively while ischemic stroke is being ruled out.
• For acute ischemic stroke, the American Heart Association recommends initiating antihypertensive therapy only if blood pressure is more than 220/120 mm Hg, or mean arterial pressure greater than 130 mm Hg. Unless there is a concerning comorbid cardiac or other condition requiring blood pressure lowering, allowing the patient's blood pressure to autoregulate at a higher level (during the acute phase) may help maximize cerebral perfusion pressure.¹⁸
• Brain imaging is recommended within 24 hours of symptom onset. While MRI with DWI is preferred, a noncontrast head CT as a widely accessible study, is a reasonable first choice when MRI is not readily available.^1,19

Consultations

• Neurologist: There is clear consensus on the need for rapid evaluation, and patients who undergo neurology evaluation and risk stratification within 24 hours versus within a few days appear to have a significantly decreased short-term risk of stroke. Therefore, decisions regarding ED evaluation, and inpatient versus rapid outpatient followup, are ideally made in concert with a neurologist. International recommendations also note that immediate consultation is more cost-effective than outpatient follow-up.¹³
• Primary care physician: This is the most important consultation that can occur, as the primary care physician will monitor the patient long term and ensure risk factor and lifestyle modification. In addition, rapid neurology consultation is not available in many communities, and the primary care doctor may well be primarily responsible for managing urgent risk stratification.
• Cardiologist: This consultation can be considered for those with clear findings that influence stroke risk, such as atrial fibrillation, patent foramen ovale, intracardiac thrombus, or valvular abnormalities.
• Vascular surgeon: This consultation should be considered for those with significant vessel stenosis or occlusion, with a goal of specialist assessment within 1 week and treatment within 2 weeks of symptom onset.^13,20,21 In many centers, some vascular interventions can be performed by other specialists including interventional radiologists, neuroradiologists, and cardiologists.

Medication

Medical management is aimed at reducing both short- and long-term risk of stroke. Antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out, given the high short-term risk of stroke following TIA. One set of guidelines from the American Stroke Association (and supported by the American Academy of Neurology) is summarized below:²²

Noncardioembolic TIA (or for those in whom no source is determined)

• Antiplatelet agents are recommended rather than oral anticoagulation as initial therapy. Aspirin (50-325 mg/d), combination aspirin/extended-release dipyridamole, and clopidogrel are all reasonable first-line options (class I recommendation).
• Combination aspirin/extended-release dipyridamole (Aggrenox) may be superior to aspirin alone (class IIa recommendation).²³
• Clopidogrel may be considered instead of aspirin alone (class IIb recommendation).
• Aspirin in combination with clopidogrel increases the risk of hemorrhage and is not routinely recommended for patients with TIA (class III recommendation). 

For those with a known cardioembolic source

• Atrial fibrillation: Long-term anticoagulation (goal INR 2-3) is typically recommended. Aspirin 325 mg/d is recommended for those unable to take oral anticoagulants.
• Acute MI with left ventricular thrombus
  • Oral anticoagulation (goal INR 2-3) is reasonable
  • Aspirin up to 162 mg/d should be used concurrently for ischemic coronary artery disease.
• Dilated cardiomyopathy: Either oral anticoagulation (goal INR 2-3) or antiplatelet therapy may be considered.
• Rheumatic mitral valve disease: Oral anticoagulation (goal INR 2-3) is reasonable. Antiplatelet agents would not normally be added to warfarin unless patients experience recurrent embolism despite a therapeutic INR.
• Mitral valve prolapse: Long-term antiplatelet therapy is reasonable.
• Mitral annular calcification: Antiplatelet therapy can be considered. Those with mitral regurgitation can be considered for warfarin or antiplatelet therapy.
• Aortic valve disease: Antiplatelet therapy may be considered.
• Prosthetic heart valves
  • For mechanical prosthetic valves, oral anticoagulants (goal INR 2.5-3.5) are recommended. For those with TIAs despite therapeutic INR, aspirin 75-100 mg/d can be added to the regimen.
  • For bioprosthetic valves, patients with TIA and no other source of thromboembolism can be considered for oral anticoagulation (INR 2-3).

Antiplatelet Agent

These agents inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. See above for recommendations for specific agents from the American Stroke Association.

Aspirin (Anacin, Ascriptin, Ecotrin, Bufferin, Bayer Aspirin)

Blocks prostaglandin synthetase action, which, in turn, inhibits prostaglandin synthesis and prevents formation of platelet-aggregating thromboxane A2.

Dosing

Adult

50-325 mg/d PO

Pediatric

10-15 mg/kg/dose PO q4-6h; not to exceed 60-80 mg/kg/d

Interactions

Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding times; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma
Because of association with Reye syndrome, do not use in children (<16 y) with flu

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants

Aspirin 25 mg/dipyridamole 200 mg

Drug combination with antithrombotic action. This combination may be superior to aspirin alone in preventing cardiovascular events following TIAs.
Aspirin irreversibly inhibits formation of cyclooxygenase, thus preventing formation of thromboxane A2, a platelet aggregator and vasoconstrictor. Platelet-inhibition lasts for life of cell (approximately 10 d).
Dipyridamole is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased cyclic-3',5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.
Each capsule contains 25 mg aspirin and 200 mg dipyridamole for total of 50 mg aspirin and 400 mg dipyridamole to be given per day.

Dosing

Adult

1 cap PO bid

Pediatric

Not established

Interactions

Theophylline may decrease hypotensive effects of dipyridamole; antiplatelet activity of dipyridamole may increase heparin toxicity
Aspirin effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; children <16 y (due to association of aspirin with Reye syndrome)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Aspirin may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
Caution in hypotension; dipyridamole has peripheral vasodilating effects

Clopidogrel (Plavix)

Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Dosing

Adult

75 mg PO qd

Pediatric

Not established

Interactions

Naproxen associated with increased occult GI blood loss; prolongs bleeding time; safety of coadministration with warfarin not established

Contraindications

Documented hypersensitivity; active pathological bleeding, such as peptic ulcer or intracranial hemorrhage

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (eg, ulcers)

Dipyridamole (Persantine)

Administer to complement usual warfarin therapy. Inhibits platelet adhesion, which may inhibit adenosine uptake by RBCs. May increase cyclic-3',5'-AMP within platelets and formation of potent platelet activator thromboxane A2. May reduce the risk of stroke when used as monotherapy instead of aspirin.

Dosing

Adult

200 mg PO bid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Theophylline may decrease hypotensive effects; because of antiplatelet effects, may increase heparin toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution with hypotension; has peripheral vasodilating effects

Ticlopidine (Ticlid)

Second-line antiplatelet therapy for patients who cannot tolerate or do not respond to aspirin therapy. In some circumstances, it can be an alternative to clopidogrel.

Dosing

Adult

250 mg PO bid

Pediatric

Not established

Interactions

Corticosteroids and antacids may decrease effects; theophylline, cimetidine, aspirin, and NSAIDs increase toxicity

Contraindications

Documented hypersensitivity; neutropenia or thrombocytopenia; liver damage; active bleeding disorders

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue if absolute neutrophil count falls to <1200/mm³ or if platelet count falls to <80,000/mm³

Anticoagulant

These agents are used to prevent venous thrombosis, pulmonary embolism, and thromboembolic disorders.

Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.

Dosing

Adult

5-15 mg/d PO for 2-5 d

Pediatric

0.05-0.34 mg/kg/d PO (infants may require doses at, or near, high end of this range)

Interactions

Many medications may impact warfarin activity
Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects of warfarin include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity; severe liver or kidney disease; open wounds; GI ulcers

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not switch brand after achieving therapeutic response; caution with active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Follow-up

Further Inpatient Care

While controversy exists regarding the need for admission, there is no controversy regarding the need for urgent evaluation, risk stratification, and initiation of stroke prevention therapy.^24,25,1

When one community implemented a strategy to ensure patients were seen within an average of 1 day, compared with an average of 3 days, the 90-day stroke risk fell from 10% to 2%.²⁶ Another initiated a program to admit patients to a "rapid evaluation unit," which dropped the 90-day stroke risk from 9.7% to 4.7%.²⁷ Others have suggested similar benefits from rapid followup.²⁸

The availability of local resources determines whether this urgent evaluation should occur as an inpatient, in an ED observation unit, or in rapid followup. In order to determine appropriate disposition, the emergency physician should determine necessary workup, then discuss with the neurologist or primary care doctor how best to ensure this occurs promptly.²⁹

One randomized controlled trial of an emergency department diagnostic protocol found that they could reduce cost, length of stay, and provide appropriate risk stratification by performing this workup in an ED observation unit (with neurology consultation) rather than in an inpatient unit.³⁰  

A number of patients present to the ED with a "transient neurological disturbance" that does not represent a true TIA, and these can be difficult to distinguish for the busy emergency practitioner. In addition, an emergent and comprehensive workup of all those with "possible TIA" may not be the most cost-effective or appropriate use of limited local resources. The emergency practitioner should use appropriate risk stratification to ensure that emergent diagnostic and therapeutic interventions are targeted to the highest risk patients. A number of risk stratification scores are available to assist in this task, but the most widely validated is the ABCD² score.^31,32,15  

ABCD² Score

The American Heart Association¹ comments "It is reasonable to hospitalize patients with TIA if they present within 72 hours of the event and any of the following criteria are present:"

• ABCD² score of 3 (Class IIa, level of Evidence C)
• ABCD² score of 0 to 2 and uncertainty that diagnostic workup can be completed within 2 days as an outpatient (Class IIa, level of Evidence C)
• ABCD² score of 0 to 2 and other evidence that indicates the patient's event was caused by focal ischemia (Class IIa, level of Evidence C)

Further Outpatient Care

• Patients selected for outpatient care should have a clear follow-up plan and stroke prevention initiated as above, including antiplatelet medication and risk factor modification.
• Patients with TIA and ipsilateral carotid artery stenosis may be candidates for urgent (<2 wk) carotid endarterectomy. In certain patients, carotid artery stenting is a reasonable alternative. This can be discussed acutely or rapid follow-up arranged.
• Patients with symptoms attributable to extracranial vertebral stenosis may be candidates for endovascular treatment, and again this should be arranged rapidly if available.

Inpatient & Outpatient Medications

• Antiplatelet agents should typically be initiated as soon as intracranial bleeding is ruled out. As above, the agent to be used varies with the patient and the specific indication.
• Antihypertensive control for those with hypertension
• Lipid control, potentially including a statin agent
• Blood glucose control for those with diabetes
• A smoking cessation strategy, which may include medication, should be initiated.
• Heavy drinkers should eliminate or reduce alcohol consumption.
• Weight loss if overweight
• Exercise

Prognosis

• With passive reporting, the early risk of stroke following TIA is approximately 4% at 2 days, 8% at 30 days, and 9% at 90 days.⁷ However, when patients with TIA are followed prospectively, the incidence of stroke is as high as 11% at 7 days.⁵
• Patients with TIAs have an increased risk of stroke and death from coronary artery disease (depending on risk factors in the study group, approximately 6-10% per year).
• Probability of stroke in the 5 years following a TIA is reported to be 24-29%.

Patient Education

• For patients to be discharged, make sure they understand the need for a complete and rapid workup through close follow-up care.
• Education regarding lifestyle modification and cardiovascular risk factors is essential.
• Education regarding stroke symptoms, the need to call emergency services immediately, and the contact number for emergency services (911 in the United States) is essential.
• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Transient Ischemic Attack (Mini-stroke).

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose an emergent alternate condition, such as brain tumor or intracranial hemorrhage
• Failure to ensure an expedited workup and initiation of stroke prevention strategies, including antiplatelet agents, given the high short-term risk of stroke

References

1. [Guideline] Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E. 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. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. Jun 2009;40(6):2276-93. [Medline].

2. Kleindorfer D, Panagos P, Pancioli A, et al. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. Apr 2005;36(4):720-3. [Medline]. [Full Text].

3. Johnston SC, Fayad PB, Gorelick PB, Hanley DF, Shwayder P, van Husen D. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. May 13 2003;60(9):1429-34. [Medline].

4. Edlow JA, Kim S, Pelletier AJ, Camargo CA Jr. National study on emergency department visits for transient ischemic attack, 1992-2001. Acad Emerg Med. Jun 2006;13(6):666-72. [Medline].

5. [Best Evidence] Giles MF, Rothwell PM. Risk of stroke early after transient ischaemic attack: a systematic review and meta-analysis. Lancet Neurol. Dec 2007;6(12):1063-72. [Medline].

6. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. Dec 13 2000;284(22):2901-6. [Medline].

7. [Best Evidence] Wu CM, McLaughlin K, Lorenzetti DL, Hill MD, Manns BJ, Ghali WA. Early risk of stroke after transient ischemic attack: a systematic review and meta-analysis. Arch Intern Med. Dec 10 2007;167(22):2417-22. [Medline].

8. Jacobs BS, Birbeck G, Mullard AJ, et al. Quality of hospital care in African American and white patients with ischemic stroke and TIA. Neurology. Mar 28 2006;66(6):809-14. [Medline].

9. White H, Boden-Albala B, Wang C, et al. Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study. Circulation. Mar 15 2005;111(10):1327-31. [Medline]. [Full Text].

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11. Kleindorfer D, Panagos P, Pancioli A, Khoury J, Kissela B, Woo D. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. Apr 2005;36(4):720-3. [Medline].

12. Cassidy JD, Boyle E, Cote P, He Y, Hogg-Johnson S, Silver FL, et al. Risk of vertebrobasilar stroke and chiropractic care: results of a population-based case-control and case-crossover study. Spine (Phila Pa 1976). Feb 15 2008;33(4 Suppl):S176-83. [Medline].

13. [Guideline] National Institute for Health and Clinical Excellence (NICE) Stroke Guidelines. Accessed November 2009. [Full Text].

14. Redgrave JN, Schulz UG, Briley D, Meagher T, Rothwell PM. Presence of acute ischaemic lesions on diffusion-weighted imaging is associated with clinical predictors of early risk of stroke after transient ischaemic attack. Cerebrovasc Dis. 2007;24(1):86-90. [Medline].

15. Prabhakaran S, Chong JY, Sacco RL. Impact of abnormal diffusion-weighted imaging results on short-term outcome following transient ischemic attack. Arch Neurol. Aug 2007;64(8):1105-9. [Medline].

16. Asimos AW, Rosamond WD, Johnson AM, Price MF, Rose KM, Murphy CV. Early diffusion weighted MRI as a negative predictor for disabling stroke after ABCD2 score risk categorization in transient ischemic attack patients. Stroke. Oct 2009;40(10):3252-7. [Medline].

17. Schwamm LH, Pancioli A, Acker JE 3rd, et al. Recommendations for the establishment of stroke systems of care: recommendations from the American Stroke Association's Task Force on the Development of Stroke Systems. Stroke. Mar 2005;36(3):690-703. [Medline].

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23. [Best Evidence] Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A. Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial. Lancet. May 20 2006;367(9523):1665-73. [Medline].

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25. Lindley RI. Patients with transient ischemic attack do not need to be admitted to hospital for urgent evaluation and treatment: against. Stroke. Apr 2006;37(4):1139-40. [Medline].

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35. Amarenco P, Labreuche J, Lavallee PC, Meseguer E, Cabrejo L, Slaoui T. Does ABCD2 score below 4 allow more time to evaluate patients with a transient ischemic attack?. Stroke. Sep 2009;40(9):3091-5. [Medline].

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Keywords

transient ischemic attack, TIA, TIA symptoms, TIA causes, TIA treatment, stroke, mini stroke, ischemic stroke, carotid artery atherosclerotic disease, vertebral artery atherosclerotic disease, brain attack, hypertension, hypotension, arteritis

Contributor Information and Disclosures

Author

Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor, Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
Joshua N Goldstein, MD, PhD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Stroke Association, Neurocritical Care Society, and Society for Academic Emergency Medicine
Disclosure: CSL Behring Consulting fee Consulting; Genentech Consulting fee Consulting

Medical Editor

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

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