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For further information, see CMDT Part 24-08: Transient Ischemic Attack

Key Features

Essentials of Diagnosis

  • Acute, focal neurologic deficit

  • Clinical deficit resolves completely within 24 hours

  • Risk factors for vascular disease often present

General Considerations

  • Focal, ischemic, cerebral neurologic deficits that last for < 24 h (usually < 1–2 h)

  • Embolization is an important etiology and may explain why separate attacks may affect different parts of the territory supplied by the same vessel

  • Cardiac embolic sources

    • Atrial fibrillation

    • Rheumatic mitral valve disease

    • Infective endocarditis

    • Atrial myxoma

    • Mural thrombi after myocardial infarction (MI)

    • Atrial septal defects and patent foramen ovale (PFO) may permit emboli from the veins to reach the brain ("paradoxical emboli")

  • Cerebrovascular sources

    • An ulcerated plaque on a major artery to the brain may be a source of emboli

    • In the anterior circulation, atherosclerotic changes occur most commonly near the carotid bifurcation extracranially and may cause a bruit

    • Other (less common) abnormalities of blood vessels that may cause transient ischemic attacks (TIAs): fibromuscular dysplasia (particularly affects the cervical internal carotid artery); atherosclerosis of the aortic arch; inflammatory arterial disorders such as giant cell arteritis, systemic lupus erythematosus, polyarteritis, and granulomatous angiitis; and meningovascular syphilis

  • Hypotension may reduce cerebral blood flow and rarely cause a TIA if a major extracranial artery to the brain is markedly stenosed

  • The subclavian steal syndrome may lead to transient vertebrobasilar ischemia from stenosis or occlusion of one subclavian artery proximal to the source of the vertebral artery

  • Hematologic causes

    • Polycythemia

    • Sickle cell disease

    • Hyperviscosity


  • Proper treatment of TIAs can help prevent strokes

  • About 30% of patients with stroke have a history of TIAs

  • Stroke develops within 90 days in 5–10% of patients with TIAs

  • Incidence of stroke is not related to the number or duration of individual TIAs but is increased in patients with hypertension or diabetes mellitus

Clinical Findings

Symptoms and Signs

  • Symptoms vary markedly among patients, but tend to be consistent in a given individual

  • Onset is abrupt, and recovery often occurs within a few minutes

  • TIA in the carotid territory may manifest with

    • Weakness and heaviness of the contralateral arm, leg, or face, singly or in combination

    • Numbness or paresthesias may occur either as sole manifestation or with motor deficits

    • Dysphagia

    • Transient monocular blindness (amaurosis fugax) may be the presenting feature when ophthalmic artery (the first branch of the internal carotid artery) is affected

    • During an attack, examination may reveal flaccid weakness with pyramidal distribution, sensory changes, hyperreflexia or an extensor plantar response on the affected side, dysphasia, or any combination of these

    • A carotid bruit or cardiac abnormality may be present

  • Vertebrobasilar TIA may manifest with

    • Vertigo

    • Ataxia

    • Diplopia

    • Dysarthria

    • Dimness or blurring of vision

    • Perioral numbness and paresthesias

    • Weakness or sensory complaints ...

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