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Transient Ischemic Attack (TIA)

By Elias A. Giraldo, MD, MS, Professor of Neurology and Director, Neurology Residency Program, University of Central Florida College of Medicine

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A transient ischemic attack is focal brain ischemia that causes sudden, transient neurologic deficits and is not accompanied by permanent brain infarction (eg, negative results on diffusion-weighted MRI). Diagnosis is clinical. Carotid endarterectomy or stenting, antiplatelet drugs, and anticoagulants decrease risk of stroke after certain types of TIA.

TIA is similar to ischemic stroke except that symptoms usually last < 1 h; most TIAs last < 5 min. Infarction is very unlikely if deficits resolve within 1 h. As shown by diffusion-weighted MRI and other studies, deficits that resolve spontaneously within 1 to 24 h are often accompanied by infarction and are thus no longer considered TIAs.

TIAs are most common among the middle-aged and elderly. TIAs markedly increase risk of stroke, beginning in the first 24 h.


Risk factors for TIA are the same as those for ischemic stroke. Modifiable risk factors include the following:

  • Alcoholism

  • Hypertension

  • Cigarette smoking

  • Dyslipidemia

  • Diabetes

  • Insulin resistance (1)

  • Obesity

  • Lack of physical activity

  • High-risk diet (eg, high in saturated fats, trans fats, and calories)

  • Psychosocial stress (eg, depression)

  • Heart disorders (particularly disorders that predispose to emboli, such as acute MI, infective endocarditis, and atrial fibrillation)

  • Use of certain drugs (eg, cocaine, amphetamines)

  • Hypercoagulability

  • Vasculitis

Unmodifiable risk factors include the following:

  • Prior stroke

  • Older age

  • Family history of stroke

  • Male sex

Most TIAs are caused by emboli, usually from carotid or vertebral arteries, although most of the causes of ischemic stroke can also result in TIAs.

Uncommonly, TIAs result from impaired perfusion due to severe hypoxemia, reduced oxygen-carrying capacity of blood (eg, profound anemia, carbon monoxide poisoning), or increased blood viscosity (eg, severe polycythemia), particularly in brain arteries with preexisting stenosis. Systemic hypotension does not usually cause cerebral ischemia unless it is severe or arterial stenosis preexists because autoregulation maintains brain blood flow at near-normal levels over a wide range of systemic BPs.

In subclavian steal syndrome, a subclavian artery stenosed proximal to the origin of the vertebral artery “steals” blood from the vertebral artery (in which blood flow reverses) to supply the arm during exertion, causing signs of vertebrobasilar ischemia.

Occasionally, TIAs occur in children with a severe cardiovascular disorder that produces emboli or a very high Hct.

Etiology reference

Symptoms and Signs

Neurologic deficits are similar to those of strokes (see Table: Selected Stroke Syndromes). Transient monocular blindness (amaurosis fugax), which usually lasts < 5 min, may occur when the ophthalmic artery is affected.

Selected Stroke Syndromes

Symptoms and Signs


Contralateral hemiparesis (maximal in the leg), urinary incontinence, apathy, confusion, poor judgment, mutism, grasp reflex, gait apraxia

Anterior cerebral artery (uncommon)

Contralateral hemiparesis (worse in the arm and face than in the leg), dysarthria, hemianesthesia, contralateral homonymous hemianopia, aphasia (if the dominant hemisphere is affected) or apraxia and sensory neglect (if the nondominant hemisphere is affected)

Middle cerebral artery (common)

Contralateral homonymous hemianopia, unilateral cortical blindness, memory loss, unilateral 3rd cranial nerve palsy, hemiballismus

Posterior cerebral artery

Monocular loss of vision (amaurosis)

Ophthalmic artery (a branch of the internal carotid artery)

Unilateral or bilateral cranial nerve deficits (eg, nystagmus, vertigo, dysphagia, dysarthria, diplopia, blindness), truncal or limb ataxia, spastic paresis, crossed sensory and motor deficits*, impaired consciousness, coma, death (if basilar artery occlusion is complete), tachycardia, labile BP

Vertebrobasilar system

Absence of cortical deficits plus one of the following:

  • Pure motor hemiparesis

  • Pure sensory hemianesthesia

  • Ataxic hemiparesis

  • Dysarthria–clumsy hand syndrome

Lacunar infarcts

*Ipsilateral facial sensory loss or motor weakness with contralateral body hemianesthesia or hemiparesis indicates a lesion at the pons or medulla.

Symptoms of TIAs begin suddenly, usually last 2 to 30 min, then resolve completely. Patients may have several TIAs daily or only 2 or 3 over several years. Symptoms are usually similar in successive carotid attacks but vary somewhat in successive vertebrobasilar attacks.


  • Resolution of stroke-like symptoms within 1 h

  • Neuroimaging

  • Evaluation to identify the cause

Transient ischemic attacks are diagnosed retrospectively when sudden neurologic deficits referable to ischemia in an arterial territory resolve within 1 h.

Isolated peripheral facial nerve palsy, loss of consciousness, or impaired consciousness does not suggest TIA. TIAs must be distinguished from other causes of similar symptoms, such as

  • Postictal [Todd] paralysis (a transient neurologic deficit, usually weakness, of the limb contralateral to the seizure focus)

Because an infarct, a small hemorrhage, and even a mass lesion cannot be excluded clinically, neuroimaging is required. Usually, CT is the study most likely to be immediately available. However, CT may not identify infarcts for > 24 h. MRI usually detects evolving infarction within hours. Diffusion-weighted MRI is the most accurate imaging test to rule out an infarct in patients with presumed TIA but is not always available.

The cause of a TIA is sought as for causes of ischemic strokes; evaluation includes tests for carotid stenosis, cardiac sources of emboli, atrial fibrillation, and hematologic abnormalities and screening for stroke risk factors. Because risk of subsequent ischemic stroke is high and immediate, evaluation proceeds rapidly, usually on an inpatient basis. It is not clear which patients, if any, can be safely discharged from the emergency department. Risk of stroke after TIA or minor stroke is highest within the first 24 to 48 h, so if either is suspected, patients are typically admitted to the hospital for telemetry and evaluation.


Treatment of transient ischemic attacks is aimed at preventing strokes; antiplatelet drugs and statins are used. Carotid endarterectomy or arterial angioplasty plus stenting can be useful for some patients, particularly those who have no neurologic deficits but who are at high risk of stroke. Anticoagulation is indicated if cardiac sources of emboli are present.

Modifying stroke risk factors, when possible, may prevent stroke.

Key Points

  • A focal neurologic deficit that resolves within 1 h is almost always a transient ischemic attack.

  • Test as for ischemic stroke.

  • Use the same treatments used for secondary prevention of ischemic stroke (eg, antiplatelet drugs, statins, sometimes carotid endarterectomy or arterial angioplasty plus stenting).

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