Transient ischemic attack (TIA) has been traditionally defined as focal neurologic symptoms attributed to a cerebrovascular territory lasting less than 24 hours.^1,2 In its recent review, the American Heart Association/American Stroke Association reports that for TIAs lasting typically minutes the presence of an infarction on magnetic resonance imaging (MRI) is not correlated with symptom duration.³ These experts redefined TIA by focal brain, spinal cord, or retinal ischemia without evidence of tissue infarction on brain imaging.³ Nevertheless, as most of the epidemiologic studies refer to it, this chapter will use the classical definition of TIA.

As brain infarction and TIA form a continuum, their mechanisms and risk factors are similar. Epidemiologic studies estimate that approximately 200,000 TIA patients present annually in the United States.^4,5 Another study from the National Hospital Ambulatory Medical Care Survey documented over 2.5 million TIAs and calculated an overall incidence rate of 1.1 per 1000 US population.⁶ In contrast to the nearly 30% reduction in the incidence of first-ever stroke, the incidence of TIA appears to be increasing based on a population based-study in the United Kingdom.⁷

In most TIAs, symptoms have resolved and physical examination is normal at the time of the clinical evaluation. Thus, the diagnosis of TIA is based on the patient’s recollection and description of symptoms. Some features, including type of symptoms (motor and language), sudden onset and short duration of symptoms, and associated vascular risk factors, can help in the clinical diagnosis.⁸ Up to 60% of patients referred to neurologists for evaluation of TIA have alternate diagnoses.^9,10,11,12 Therefore, agreement on a TIA clinical diagnosis remains poor, even among stroke neurologists, whose judgments are often considered the gold standard.^13,14 With the advent of diffusion-weighted imaging (DWI) and computed tomography (CT) or MR perfusion imaging, the finding of cytotoxic injury (restricted diffusion) or focal hypoperfusion in patients evaluated for suspicion of TIA provides convincing evidence of brain ischemia.^{15,16,17,18,19,20} Therefore, the combination of a specialized clinical evaluation with advanced neuroimaging is the mainstay of TIA evaluation.³

TIA diagnosis is an emergency because the risk of stroke after a TIA is high (20% at 3 months)²¹ and approximately half of this risk occurs within the first 48 hours of TIA symptoms.^22,23,24 Several tools exist to estimate the risk of stroke after TIA. The ABCD2 (Age, Blood pressure, Clinical symptom type, Duration of symptoms, and Diabetes) score is a simple clinical scale that evaluates the characteristics of a TIA. In the referent publication, the risk of stroke at 2 days associated with ABCD2 score was, respectively, for a score of six or seven, 8.1%, four or five, 4.1%, and zero to three, 1.0%. Therefore, an ABCD2 score above three has been chosen to decide patient hospitalization.¹⁵ The ABCD2 score has become the standard tool to estimate the risk of stroke after a TIA.²⁵ Nevertheless, this score accurately predicts stroke in only 60% of patients and, therefore, may not be considered by itself a reliable tool to triage TIA patients.^26,27,28 The detection of tissue infarction or symptomatic brain or neck vessel stenosis represents independent risk factors of stroke.^{16,19,26,29,30,31,32} The incorporation of brain infarction and symptomatic vessel stenosis into the ABCD2 score increases its ability to predict the risk of future stroke by almost 15%.^31,32