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 and nonbacterial thrombotic 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; Fabry disease; 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

Demographics

• 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 ...