ESSENTIALS OF DIAGNOSIS
Focal neurologic deficit of acute onset.
Clinical deficit resolves completely within 24 hours.
Risk factors for vascular disease often present.
Transient ischemic attacks (TIAs) are characterized by focal ischemic cerebral neurologic deficits that last for less than 24 hours (usually less than 1–2 hours). About 30% of patients with stroke have a history of TIAs and 5–10% of patients with TIAs will have a stroke within 90 days. The natural history of attacks is variable. Some patients will have a major stroke after only a few attacks, whereas others may have frequent attacks for weeks or months without having a stroke. The risk of stroke is high in the first 3 months after an attack, particularly in the first month and especially within the first 48 hours. The stroke risk is greater in patients older than 60 years, in patients with diabetes, or after TIAs that last longer than 10 minutes and with symptoms or signs of weakness, speech impairment, or gait disturbance. In general, carotid ischemic attacks are more liable than vertebrobasilar ischemic attacks to be followed by stroke.
Urgent intervention in TIA patients reduces rates of subsequent stroke, and the condition should be treated with a similar sense of urgency as unstable angina.
An important cause of transient cerebral ischemia is embolization. In many patients with these attacks, a source is readily apparent in the heart or a major extracranial artery to the head, and emboli sometimes are visible in the retinal arteries. An embolic phenomenon explains why separate attacks may affect different parts of the territory supplied by the same major vessel. Cardiac causes of embolic ischemic attacks include atrial fibrillation, heart failure, infective and nonbacterial thrombotic endocarditis, atrial myxoma, and mural thrombi complicating myocardial infarction. Atrial septal defects and patent foramen ovale may permit venous thromboemboli to reach the brain (paradoxical emboli). An ulcerated plaque on a major artery to the brain may serve as a source of emboli. In the anterior circulation, atherosclerotic changes occur most commonly in the region of the carotid bifurcation extracranially; these changes may cause a bruit. Atherosclerosis also affects the vertebrobasilar system and the major intracranial vessels including the middle and anterior cerebral arteries.
Less common abnormalities of blood vessels that may cause TIAs include fibromuscular dysplasia, which affects particularly the cervical internal carotid artery; atherosclerosis of the aortic arch; inflammatory arterial disorders such as giant cell arteritis, polyarteritis, and granulomatous angiitis; and meningovascular syphilis. Critical stenosis of a major extracranial or intracranial artery may cause TIA, especially in the setting of hypotension.
Hematologic causes of TIA include polycythemia, sickle cell disease, hyperviscosity syndromes, and the antiphospholipid antibody syndrome. Severe anemia may also lead to transient focal neurologic deficits in patients with preexisting cerebral arterial disease.
The subclavian steal syndrome may lead to ...