Transient ischemic attacks are focal neurologic episodes that correspond to a vascular territory, appear abruptly and cease in matter of minutes. Previously, the definition on clinical grounds extended to spells that lasted up to 24 h, then a shorter time frame was adopted but now, an event that leaves no clinical or imaging trace of infarction is considered a TIA. It has been realized as a result of more sophisticated techniques that many TIAs previously attributed to atherothrombosis, are truly embolic strokes that resolve clinically. These episodes can reflect the involvement of virtually any cerebral artery: common or internal carotid; middle, posterior, or anterior cerebral; ophthalmic; vertebral, basilar, or cerebellar; or a penetrating branch to the internal capsule, thalamus, or brainstem. Thus, TIAs may present themselves as transient spells of hemiparesis, aphasia, numbness, or tingling on one side of the body, dysarthria, diplopia, ataxia, obscuration of a visual field, or combinations thereof that replicate the stroke syndromes. Even limb shaking can represent a TIA (Yanagihara et al). Although there is little doubt that TIAs are caused by transient focal ischemia, their mechanism is not fully understood.
Transient ischemic episodes must be distinguished from other brief neurologic attacks that are from seizures, migraine, and its variants, transient global amnesia, syncope, vertigo from labyrinthine disease, and psychogenic episodes, as emphasized further on. The differentiation of TIAs from other similar transient spells is not always straightforward and occupies considerable attention from neurologists; these distinctions have serious implications with regard to evaluation and treatment.
In the clinical analysis of TIAs, it is useful to separate a single transient episode from repeated ones that are all of uniform type. The latter are more a warning of impending vascular occlusion, particularly of the internal carotid artery, whereas the former, especially when prolonged, are again often caused by an embolus that leaves no lasting clinical effect. Prolonged, fluctuating TIAs are the most ominous. Approximately 20 percent of infarcts that follow TIAs occur within a month after the first attack, and approximately 50 percent within a year (Whisnant et al). In an attempt to provide a predictive tool, various scales were devised, among them the “ABCD” system devised by Rothwell and colleagues (2005) and derivatives of this scale. Blood pressure, unilateral weakness, speech disturbance, and the duration of symptoms (all less than 1 h) are added to produce a predictive score for stroke within 1 week. Studies subsequent to the original one have given variable sensitivities, for which reason this interesting approach must be considered in clinical context. In the original study, unilateral weakness and duration lasting over an hour were most predictive of stroke. The problem of determining the cause of a prolonged TIA has been alluded to—many of these cases are a result of emboli.
Not surprisingly, the rates of myocardial infarction and other atherosclerotic events such as myocardial infarction are high in patients with TIAs, in some series exceeding the risk of stroke. About two-thirds of all patients with TIAs are men with hypertension, reflecting the higher incidence of atherosclerosis in this group. Occasionally, in younger adults, TIAs may occur as relatively benign phenomena, without recognizable features of atherosclerosis or risk factors for it. Migraine is suspected in such patients (see further on); other such instances are a result of special hematologic disorders such as those that cause excessive viscosity or sludging of blood (polycythemia vera, sickle cell disease, thrombocytosis, leukemia, and hyperglobulinemic states) may also cause TIAs prior to a stroke.