Nanda, A, Niranjan NS, Transient Ischemic Attack. Medscape.

2013

A transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction that typically
lasts less than an hour; results from focal cerebral, spinal cord, or retinal ischemia; and is not associated
with acute tissue infarction.[1] In people who have a TIA, the incidence of subsequent stroke is as high as
11% over the next 7 days and 24-29% over the following 5 years. [2]

Essential update: CT scanning may demonstrate high stroke risk following TIA
A study by Wasserman et al indicated that in patients who have had a TIA or nondisabling stroke,
computed tomography (CT) scanning, by finding evidence of acute ischemia, can be used to determine
which of them have a high stroke risk. The study involved 2028 patients who underwent CT scanning
within 24 hours of a TIA or nondisabling stroke. The investigators found that the stroke risk was high in
patients whose baseline CT scan indicated the presence of acute ischemia (10.6%) and was even higher
if, in addition to acute ischemia, the patient had chronic ischemia (17.4%) or microangiopathy (17.6%).
Having all three risk factors was associated with a 25% stroke rate. The study also reported that patients
with evidence of acute ischemia had a three-fold higher stroke rate in the first 2 days than did the other
patients.[3, 4]

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 patients 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
theNational 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 patients 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
Ruling out metabolic or drug-induced etiologies for symptoms consistent with a TIA is important. 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) [5]
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 [5, 6] :

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[5, 2, 7, 8] :

Evaluation
Risk stratification (eg, with the California or ABCD score [5] )
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) [8]
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.

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. [1] 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, 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.[5]

Clinical assessment of possible TIA involves careful investigation of the onset, duration, fluctuation,
location, and intensity of symptoms. Reviewing the patients 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 patients 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). [5, 9] (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.

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 occlusiontypically, from an acute thromboembolic
eventor 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).

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
Epidemiology
Between 200,000 and 500,000 TIAs are diagnosed annually in the United States. [10, 11] 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.[12] 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.
[13]
TIAs occur in about 150,000 patients per year in the United Kingdom. [2] 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. [10] 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).[14]

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. [1,
8]

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.[15] When patients with TIA are followed prospectively, however, the incidence of stroke
is as high as 11% at 7 days.[2] 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. [16]

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.[17]

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).