Transient ischemic attack (TIA) is traditionally defined as a transient, reversible localized cerebral blood circulation disorder with complete resolution of signs and symptoms within 24h. However, with the development of imaging, many patients with TIA meeting the traditional definition have evidence of cerebral infarction. It has been found that the 24-h criterion for the diagnosis of TIA no longer meets the practical needs. The latest definition of TIA is a transient episode of neurological deficit due to localized brain tissue or retinal ischemia, with typical clinical symptoms lasting no more than 1 h, and without clear evidence of acute cerebral infarction. Ischemic stroke should be diagnosed if clinical symptoms persist and there are characteristic imaging signs consistent with acute ischemic stroke. Zhang Yi, Department of Tui Na, Xinjiang Uygur Autonomous Region Hospital of Traditional Chinese Medicine The clinical features of TIA include: ① sudden onset. (2) Focal ischemic symptoms in the brain or retina. The average duration of TIA is 14 min in the internal carotid system and 8 min in the vertebral basilar artery system, and most of them resolve within 1 h. ④The recovery is complete, and there are no symptoms of neurological deficit during the remission period; ⑤Recurrent attacks. There are many theories about the pathogenesis of TIA: cerebral vasospasm, microembolism, hemodynamic changes, etc. Hemodynamic alteration theory: When a certain artery is narrowed or occluded, the effect on cerebral blood supply is small when the vessel is mildly narrowed, but when the narrowing is ≥50% or even 70% or more, it will affect the hemodynamics and lead to the occurrence of hypoperfusion TIA. Especially when the systemic blood redistribution or blood pressure decreases, the blood flow to the site of severe stenosis will be even more reduced, and TIA will recur, and even cerebral infarction will occur. Microembolism theory: Atherosclerotic plaque of carotid artery or cerebral artery and the debris of thrombus clot attached to the wall when ulceration occurs → cerebral microembolism → local ischemic symptoms → distal vasodilatation of embolus movement or embolus autolysis → blood supply is restored and symptoms disappear. It can be seen that the occurrence of TIA is not only related to carotid stenosis, but also closely related to the instability of carotid atherosclerotic plaque, i.e., plaque rupture, plaque ulceration, and inflammation at the plaque site. Unstable plaque: the risk of rupture is high, and the risk of thrombosis is also high, which makes it easy to form embolic infarction or embolic TIA. Stable plaque: its risk may be related to the hemodynamic changes caused by the stenosis of plaque formation, which makes it easy to form hypokinetic infarction or hypokinetic TIA. The main clinical characteristics of TIA are transient, localized and recurrent, therefore, the traditional concept is that, Therefore, the traditional concept is that TIA is a “benign and reversible ischemic syndrome”. However, modern studies have found that the risk of secondary stroke is 8% within 7 days, 10% within 30 days, and 10% to 20% within 90 days after the onset of TIA, with an average of 11%. The risk of recurrent stroke within 90 days of acute stroke is only 2%-7%, with a mean of 4%, which is significantly lower than that of TIA. TIA and ischemic stroke share the same pathophysiological basis, and TIA is the most important independent risk factor for ischemic stroke. The progression from TIA to ischemic stroke is a continuous and gradual process. A growing number of studies have bundled TIA, mini-stroke and stroke together, blurring the boundaries between them. In recent years, as clinical research has progressed and a large number of clinical cases have been accumulated, it has been found that about 50% of stroke patients have a history of TIA before the onset of stroke. In 2010, the Chinese Journal of Neurology published the Guidelines for the Secondary Prevention of Ischemic Stroke and Transient Ischemic Attack 2010. It also reflects the recognition and importance of these two diseases in the medical field. How to diagnose and treat TIA has become a problem and a hot spot in the current brain disease medicine. Currently, the most effective ways to diagnose TIA are imaging and symptomatology records. Conventional CT and MRI are not sensitive enough for the ischemic changes of the brain in TIA, while perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) can show these processes. Clinical studies have shown that approximately 1/2 of patients with TIA have clinically relevant lesions on DWI, and 1/2 of them do have infarct foci visible on subsequent MRI. The treatment of TIA is mainly focused on anticoagulation and relative treatment for the cause. If necessary, surgery can be used to restore the blood supply to the brain. We hope that all patients will recognize and pay attention to the seriousness of TIA, prevent and treat it early, improve the quality of life and prevent the occurrence of stroke.