Transient ischemic attack (TIA) describes neurologic symptoms of ischemic origin that last less than 24 hours. In fact, most attacks last only a few minutes to an hour. Often called a mini-stroke, a TIA may have ominous implications. About one in three people who have stroke risk factors and experience an authentic TIA will eventually have a stroke during their lifetime, with about half occurring within a year of the initial TIA.

TIAs have more than one mechanism. When severe carotid or vertebrobasilar stenosis is present, transient ischemia can be caused by low flow distally; such TIAs are typically brief and stereotyped, presenting with repeated episodes of the same syndrome. TIAs of this hemodynamic type may occur only during upright posture or during transient hypotension or cardiac arrhythmia. When TIAs are caused by embolism—from the heart, aorta, or proximal large-vessel atherosclerotic plaque or dissection—they may last longer, as the embolus transiently occludes a distal arterial branch before spontaneously dissolving. Less commonly, permanent small-vessel occlusion with evidence of a small infarct on magnetic resonance (MR) diffusion-weighted imaging (DWI) can result in a transient deficit lasting up to 24 hours before resolving (“cerebral infarction with transient symptoms”). A newer “tissue-based” definition of TIA restricts the diagnosis to brief episodes of focal neurologic dysfunction—typically less than 1 hour—without imaging evidence of acute infarction on computed tomography (CT) or MR imaging.

Small-vessel TIAs may result from lipohyalinosis and arteriolosclerosis of small penetrating vessels, such as the lenticulostriate branches of the middle cerebral artery, or penetrators of the vertebral and basilar arteries. Intracranial or extracranial arterial dissection may produce hemodynamic compromise or embolism. Fibromuscular dysplasia and Ehlers-Danlos type IV predispose to dissection. Vasospasm-related TIA may respond to calcium channel blockers.

TIAs have also been associated with hyperviscosity—polycythemia, sickle cell anemia, and thrombocythemia as well as with cerebral venous thrombosis, bacterial endocarditis, and temporal arteritis— and may clear with correction of these underlying disorders. TIAs in cocaine users may be the result of drug-induced cerebral vasospasm.

Symptoms vary with the arterial territory involved. Transient monocular blindness (TMB or amaurosis fugax) due to ischemia in the territory of the central retinal artery consists of blurring or darkening of vision, peaking within a few seconds (sometimes as if a curtain had descended) and usually clearing within minutes. The most important cause of TMB is proximal internal artery stenosis producing either hemodynamic compromise or embolism. Hollenhorst plaques resulting from cholesterol microemboli may be seen in retinal artery branches.

Carotid territory TIAs that involve the brain produce varying combinations of limb weakness and sensory loss, aphasia, or hemineglect. Posterior circulation TIAs cause symptoms referable to the cerebrum (visual field loss or cortical blindness), brain stem (cranial nerve and long-tract symptoms, sometimes crossed or bilateral), and cerebellum. Some TIAs produce transient “lacunar syndromes” such as pure hemiparesis or pure hemisensory loss. TIAs can cause paroxysmal dyskinesias, including tremor, ataxia, limb dystonia, and myoclonic jerking. Coarse irregular shaking of an arm or leg lasting seconds to a minute, so-called limb-shaking TIA, and sometimes precipitated by a change to upright posture, is often associated with critical carotid artery stenosis or occlusion. Although rare, high-grade stenosis or complete occlusion of both internal carotid arteries and the proximal basilar artery can lead to “drop attacks.”

In the subclavian steal syndrome, stenosis of the subclavian or innominate artery proximal to the origin of the vertebral artery leads to brain stem, cerebellar, or even cerebral symptoms, often manifested during exertion and sometimes accompanied by symptoms of arm claudication. The syndrome results from diversion of anterograde flow via the patent vertebral artery retrograde down the contralateral vertebral artery distal to the occlusion, depriving the basilar artery of blood flow.

Recurrent TIAs of the same type are more likely to be the result of perfusion failure due to critical narrowing or occlusion of the involved artery than of embolism.