It has been half a century since the concept of transient ischemic attack (TIA) was first proposed by Fisher. With the rapid development of neuroscience and imaging in recent years, people have gained a deeper understanding of TIA, and many new concepts have emerged in terms of concept, etiology, imaging, clinical manifestations, treatment and prognosis. 1. Traditional concept and modern understanding of TIA In 1965, the Fourth Princeton Conference defined the definition of TIA: symptoms of neurological deficits due to focal or regional ischemia of the brain, and disappear completely within 24 hours. That is, brain parenchymal injury can occur when symptoms persist for more than 24 hours, thus distinguishing TIA from cerebral infarction. However, large-scale studies have shown that the duration of typical TIA symptoms is generally several minutes to 1 hour, so many scholars have suggested changing the time limit of TIA to 1 hour, which is still controversial. In recent years, several studies have been pooled, and brain parenchymal damage can be present on CT and MRI in patients with TIA longer than 1 hour. Diffusion-weighted imaging (DWI) studies have shown that ischemic lesions are present on DWI images in half of the patients who meet the traditional definition of TIA, and in 1/2 of these cases, cerebral infarct foci are visible on subsequent imaging, such as T2-weighted (T2WI) MRI [1]. To accommodate clinical needs, Albers et al. of Stanford University School of Medicine suggested the following new definition: TIA is a transient episode of neurological dysfunction caused by focal cerebral or retinal ischemia, with clinical symptoms typically lasting less than 1 hour and without clear evidence of acute ischemic stroke [2]. Ischemic stroke should be diagnosed if clinical symptoms persist and there are characteristic imaging findings consistent with acute ischemic stroke. The presence or absence of ischemic damage to the brain or retina is also proposed as a basis for the diagnosis of TIA. In view of the fact that MRI is not widely available in some hospitals and it is difficult to distinguish the above concepts by CT alone, some scholars such as Ballotta [3] proposed the concept of “transient stroke” instead of TIA. In 2003, Kidwell et al [4] proposed a new concept -This concept is still under discussion, but it certainly provides a more reasonable explanation for the traditional definition of TIA. Since AICS covers TIA, some scholars also believe that it is only a matter of time before TIA is abandoned [5]. All this will shake the clinicians’ traditional concept of TIA. 2. Imaging of TIA Previously, CT was the main method used for the examination and differential diagnosis of TIA. Some [6] reported that 69% of patients with TIA had normal head CT, 26% had old lesions, and only 5% could find new lesions, usually in those with longer duration of symptoms.MRI examination is more sensitive than CT. MRI has been reported to detect infarct foci in 77-84% of TIA patients, but some of these foci are not associated with acute damage [7]. The last two examinations have limited evaluation of TIA and cannot distinguish acute from chronic ischemic lesions and their relationship with TIA. With the development of imaging, especially the application of functional magnetic resonance techniques, the understanding of TIA has been further improved. It has been shown [8] that when TIA is mildly focal ischemia PWI can detect a decrease in local cerebral blood flow, but no abnormalities are shown on DWI and T2WI; when TIA is more severe PWI and DWI both show abnormalities, while T2WI has no abnormalities; when ischemia is more severe PWI, DWI and T2WI all show abnormal signals. DWI can detect extracellular ischemia in the brain after several minutes of ischemia Inatomi et al [9] concluded that 44% of patients with TIA had abnormal DWI, and that the duration of TIA ≥30 min was significantly more positive than that of DWI <30 min. The positivity rate is significantly increased. 3. Clinical manifestations of TIA Classic TIA manifestations include symptoms of the internal carotid artery system: hemianesthesia, weakness, speech impairment, blackness and monocular visual impairment; symptoms of the vertebrobasilar artery system: vertigo, balance disorders, diplopia, dysphagia, crossed sensory and motor impairment. Less common symptoms include: psychiatric symptoms, impaired consciousness, hemiparetic chorea-like episodes, transient generalized amnesia (TGA), fall episodes, visual and facial disorientation. It should be noted that transient loss of consciousness, although seen in TIA, is more commonly seen in syncope and epilepsy, as vertebrobasilar artery occlusion often has other concomitant symptoms, such as signs of oculomotor and muscle movement disorders. Falling episodes have been inappropriately attributed to transient ischemia of the posterior circulation. In the absence of signs and symptoms suggestive of brainstem or cerebellar dysfunction, ischemia of the posterior circulation is rarely the cause of a fall attack [10]. Impairments in intelligence, reasoning and abstract thinking, attention, language, computation and memory can occur after TIA in either the internal carotid system or the vertebrobasilar system, most notably memory impairment. Many literatures have pointed out that TIA is an important risk factor for vascular dementia, which can accelerate the process of brain degeneration and cognitive decline [11]. 4. Treatment of TIA Before treating TIA, it is important to comprehensively analyze the risk factors present, the pathogenesis, select the appropriate treatment plan and judge the prognosis. The most important of the control of risk factors is the regulation of blood pressure, which is still a major controversy. The 1999 AHA guidelines [12] recommend controlling blood pressure below 140/90 mmHg in general and below 130/85 mmHg in diabetic patients. 2003 Rothwell [13] and others showed that the risk of stroke is significantly higher in patients with unilateral or bilateral severe carotid stenosis with systolic blood pressure <130 mmHg, and at this time, if the The risk of stroke is significantly higher in patients with systolic blood pressure <130 mmHg in unilateral or bilateral severe carotid stenosis. Therefore, when unilateral carotid stenosis is present, systolic blood pressure should be maintained above 130 mmHg; when both carotid arteries are severely stenosed, systolic blood pressure should be maintained at least above 150 mmHg. It can be seen that antihypertensive drugs should be used with caution in hemodynamic TIA, while all other types of TIA should be antihypertensive. Based on the results of recent large-scale clinical trials, it is recommended that aspirin (50-325 mg/d) remains the first choice for patients with non-cardiogenic TIA, and other antiplatelet agents such as ticlopidine, clopidogrel and disopyramide can also be used as first-line therapeutic agents. Again, warfarin therapy (INR 2.0-3.0) should be recommended for anticoagulation in patients with cardiogenic TIA, and its prevention of cardiogenic embolism is significantly better than that of aspirin. The results of several studies [14,15] showed no significant difference between the efficacy of anticoagulation and antiplatelet therapy in non-cardiogenic TIA and that anticoagulation can increase the risk of bleeding. However, some authors believe [10] that anticoagulation may be considered in patients with severe large artery stenosis and arterial entrapment. In patients with TIA with atherosclerotic plaques, statins can be applied, even in the absence of lipid metabolism disorders, presumably related to their atherosclerotic plaque stabilizing effect [16]. In patients with hemodynamic TIA caused by carotid stenosis, when the stenosis is between 70% and 99%, benefit from carotid endarterectomy (CEA), but it is closely related to the clinical experience of the operator [17]. In recent years, endovascular interventions have been applied to patients with TIA, including: carotid stenting (CAS), vertebrobasilar stenting, and intracranial artery stenting, but there are no direct large-scale comparative studies of CEA and CAS. 5. Prognosis of TIA Traditionally, it is believed that 1/3 of patients get remission after TIA, 1/3 of patients still have recurrent attacks, and 1/3 of patients will develop stroke. Recent evidence suggests that the risk of stroke in patients with TIA exceeds 10-20% within 90 d, with the highest risk occurring in the first 2 d after onset [18]. patients with TIA are at high risk not only for cerebral infarction but also for myocardial infarction and sudden death. Prognostic factors suggesting a high risk include: severe carotid stenosis (70%-99%), ipsilateral plaque rupture, high suspicion of cardiac emboli origin, hemispheric TIA, age >65 years in men, 2 TIAs <24h apart, and combination of other risk factors. After the diagnosis of TIA is made, the prognosis should be evaluated according to the above risk factors and treatment measures should be actively taken as early as possible. 6. Conclusion With the continuous progress of medicine, the concept of TIA has undergone new changes in recent years. It is expected that the definition and some of the views of TIA will be revised in the near future, and the etiological treatment of TIA should be emphasized and secondary prevention should be carried out effectively in order to further reduce the occurrence of ischemic stroke.