Transient Ischemic Attack

Updated: Sep 11, 2017
  • Author: Ashish Nanda, MD; Chief Editor: Andrew K Chang, MD, MS  more...
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Overview

Practice Essentials

In 2009, the American Heart Association and the American Stroke Association (AHA/ASA) published a scientific statement that revised the definition of transient ischemic attack (TIA) to the following:  "a transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction." [1]  Prior to this revised definition, TIA was often operationally defined based on symptom duration lasting less than 24 hours, with typical episodes lasting less than 1 hour. The de-emphasis on duration was due to multiple studies demonstrating that up to 50% of classically defined TIAs showed brain injury on magnetic resonance imaging (MRI).  

On average, the annual risk of future ischemic stroke after a TIA or initial ischemic stroke is 3–4%, [2] with an incidence as high as 11% over the next 7 days and 24–29% over the following 5 years. [3]

Signs and symptoms

A TIA may last only minutes, and symptoms often resolve 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 regarding changes in any of the following:

  • Behavior
  • Speech
  • Gait
  • Memory
  • Movement

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

The goals of the physical examination are to uncover any neurologic deficits, to evaluate for underlying cardiovascular risk factors, and to 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 neurologic examination is the foundation of the TIA evaluation and should focus in particular on the neurovascular distribution suggested by the patient’s symptoms. Subsets of the neurologic examination include the following:

  • Cranial nerve testing
  • Determination of somatic motor strength
  • Somatic sensory testing
  • Speech and language testing
  • Assessment of the cerebellar system (be sure to watch the patient walk)

See Presentation for more detail.

Diagnosis

It is important to rule out other causes, such as metabolic or drug-induced etiologies, which can present with symptoms similar to that of TIA. The following tests are considered on an emergency basis:

  • A fingerstick blood glucose for hypoglycemia
  • Complete blood count
  • Serum electrolyte levels
  • Coagulation studies
  • 12-lead electrocardiogram (ECG) with rhythm strip

The following tests typically are helpful and often can be performed on an urgent basis:

  • Erythrocyte sedimentation rate
  • Cardiac enzymes
  • Lipid profile

Additional laboratory tests, ordered as needed and on the basis of the history, include the following:

  • Screening for hypercoagulable states (particularly in younger patients with no known vascular risk factors) [1]
  • Syphilis serology
  • Antiphospholipid antibodies
  • Toxicology screens
  • Hemoglobin electrophoresis
  • Serum protein electrophoresis
  • Cerebrospinal fluid examination

Imaging of the brain should be performed within 24 hours of symptom onset, as follows [1, 4] :

  • Magnetic resonance imaging (MRI) with diffusion-weighted imaging (preferred)
  • Noncontrast computed tomography (CT; ordered if MRI is not available)

The cerebral vasculature should be imaged urgently, preferably at the same time as the brain. Vascular imaging for TIA includes the following:

  • Carotid Doppler ultrasonography of the neck
  • CT angiography (CTA)
  • Magnetic resonance angiography (MRA)

See Workup for more detail.

Management

The following should be done urgently in patients with TIA [1, 3, 5, 6] :

  • Evaluation
  • Risk stratification (eg, with the California or ABCD score [1] )
  • Initiation of stroke prevention therapy

For patients with a recent (≤1 week) TIA, guidelines recommend a timely hospital referral with hospitalization for the following:

  • Crescendo TIAs
  • Duration of symptoms longer than 1 hour
  • Symptomatic internal carotid stenosis greater than 50%
  • Known cardiac source of embolus (eg, atrial fibrillation)
  • Known hypercoagulable state
  • Appropriate combination of the California score or ABCD score (category 4) [6]

In view of the high short-term risk of stroke after TIA, antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out. For noncardioembolic TIA, the following antiplatelet agents are all reasonable first-line options for initial therapy:

  • Aspirin (50-325 mg/day)
  • Aspirin plus extended-release dipyridamole
  • Clopidogrel

Stroke prevention medication typically recommended for cardioembolic TIA is as follows:

  • For patients with atrial fibrillation after TIA, long-term anticoagulation with warfarin (target international normalized ratio [INR], 2-3); aspirin 325 mg/day for those unable to take oral anticoagulants
  • In acute myocardial infarction (MI) with left ventricular thrombus, oral anticoagulation with warfarin (target INR, 2-3; concurrent aspirin up to 162 mg/day for ischemic coronary artery disease [CAD])
  • In dilated cardiomyopathy, oral anticoagulation with warfarin (target INR, 2-3) or antiplatelet therapy
  • In rheumatic mitral valve disease, oral anticoagulation with warfarin (target INR, 2-3)

For patients with TIA due to 50-99% stenosis of a major intracranial artery, the following is recommended:

  • Aspirin 50-325 mg/day rather than warfarin
  • Maintenance of blood pressure below 140/90 mm Hg and total cholesterol below 200 mg/dL
  • Angioplasty or stent placement is investigational and of unknown utility

See Treatment and Medication for more detail.

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Background

A transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction that results from focal cerebral, spinal cord, or retinal ischemia, and is not associated with acute tissue infarction. [7] The clinical symptoms of TIA typically last less than 1 hour and often last for less than 30 minutes, but prolonged episodes can occur.

Whereas the classical definition of TIA included symptoms lasting as long as 24 hours, advances in neuroimaging have suggested that many such cases represent minor strokes with resolved symptoms rather than true TIAs. Thus, in 2009 the American Heart Association (AHA) and the American Stroke Association (ASA) endorse a tissue-based definition of TIA (ie, as an episode of focal ischemia rather than acute infarction) rather than a time-based definition. [1]

Clinical assessment of possible TIA involves careful investigation of the onset, duration, fluctuation, location, 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 can be a reliable resource for insights into previous episodes and workup.

A neurologic examination is the foundation of the TIA evaluation and should focus in particular on the neurovascular distribution suggested by the patient’s symptoms. (See Presentation.)

Initial assessment is aimed at excluding emergency conditions that can mimic a TIA, which include the following:

  • Hypoglycemia
  • Seizure
  • Tumor or mass lesion
  • Migraine with aura
  • Peripheral nerve/root disorder
  • Demyelinating disease
  • Vestibular dysfunction
  • Intracranial hemorrhage
  • Electrolyte derangements

Thus, a fingerstick blood glucose test should be performed to check for hypoglycemia, and blood should be drawn for laboratory studies. The following tests are considered on an emergency basis: serum chemistry profile, including creatinine; coagulation studies; and complete blood count (CBC). [1, 8] (See Workup.)

Antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out. (See Treatment and Medication .)

For more information, see Ischemic Stroke in Emergency Medicine.

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Pathophysiology

TIAs are characterized by a temporary reduction or cessation of cerebral blood flow in a specific neurovascular distribution as a result of partial or total occlusion—typically, from an acute thromboembolic event—or stenosis of a small penetrating vessel. Clinical manifestations will vary, depending on the vessel involved and the cerebral territory it supplies (see Ischemic Stroke in Emergency Medicine).

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Etiology

The TIA workup should focus on emergency/urgent risk stratification and management. Numerous potential underlying causes can be readily identified, including the following:

  • Atherosclerosis of extracranial carotid and vertebral or intracranial arteries
  • Embolic sources - Valvular disease, ventricular thrombus, or thrombus formation from atrial fibrillation, aortic arch disease, paradoxical embolism via a patent foramen ovale (PFO) or atrial-septal defect (ASD)
  • Arterial dissection
  • Arteritis - Inflammation of the arteries occurring primarily in elderly persons, especially women; noninfectious necrotizing vasculitis (primary cause); drugs; irradiation; local trauma; connective tissue diseases
  • Sympathomimetic drugs (eg, cocaine)
  • Mass lesions (eg, tumors or subdural hematomas) – These less frequently cause transient symptoms and more often result in progressive persistent symptoms
  • Hypercoagulable states (eg, genetic or associated with cancer or infection)

Causes in children

TIA etiologies in children, which can differ from those in adults, include the following:

  • Congenital heart disease with cerebral thromboembolism (most common)
  • Drug abuse (eg, cocaine)
  • Clotting disorders
  • Central nervous system infection
  • Neurofibromatosis
  • Vasculitis
  • Idiopathic progressive arteriopathy of childhood (moyamoya)
  • Fibromuscular dysplasia
  • Marfan disease
  • Tuberous sclerosis
  • Tumor
  • Sickle cell disease
  • Focal arteriopathies
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Epidemiology

Between 200,000 and 500,000 TIAs are diagnosed annually in the United States. [9, 10] Emergency department (ED) visits for TIAs occur at an approximate rate of 1.1 per 1000 US population, and TIAs are diagnosed in 0.3% of ED visits. [11] TIA carries a particularly high short-term risk of stroke, and approximately 15% of diagnosed strokes are preceded by TIAs.

Internationally, the probability of a first TIA is around 0.42 per 1000 population in developed countries. [12] TIAs occur in about 150,000 patients per year in the United Kingdom. [3] The incidence likely mirrors that of stroke.

The incidence of TIAs increases with age, from 1-3 cases per 100,000 in those younger than 35 years to as many as 1500 cases per 100,000 in those older than 85 years. [9] Fewer than 3% of all major cerebral infarcts occur in children. Pediatric strokes often can have quite different etiologies from those of adult strokes and tend to occur with less frequency.

The incidence of TIAs in men (101 cases per 100,000 population) is significantly higher than that in women (70 per 100,000). [13]

The incidence of TIAs in blacks (98 cases per 100,000 population) is higher than that in whites (81 per 100,000 population). Controversy exists regarding whether race influences emergency workup after TIA. [7, 6]

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Prognosis

With passive reporting, the early risk of stroke after TIA is approximately 4% at 2 days, 8% at 30 days, and 9% at 90 days. [14] When patients with TIA are followed prospectively, however, the incidence of stroke is as high as 11% at 7 days. [3] The probability of stroke in the 5 years following a TIA is reported to be 24-29%. In addition, patients with TIAs or stroke have an increased risk of coronary artery disease. [15]

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Patient Education

Before being discharged from the hospital, patients who have been diagnosed with TIA must receive clear instruction to ensure that they understand the need for a complete and rapid workup through close follow-up care. Also essential for patients is education on stroke symptoms, the need to call emergency services immediately if any of these symptoms occur, and the contact number for emergency services (911 in the United States and Canada).

Despite program efforts in public education, many patients still do not seek medical attention after experiencing TIA symptoms. A 2010 population-based study found that 31% of all patients who experienced a recurrent stroke within 90 days of their first TIA or minor stroke had not sought medical attention after the initial event. [16]

Public health professionals and physicians need to do more, such as promoting and participating in medical screening fairs and public outreach programs. In addition, patients need to be educated about lifestyle modification and cardiovascular risk factors.

For patient education information, see the Stroke Center, as well as Transient Ischemic Attack (Mini-stroke).

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