Transient ischemic attack (TIA) is traditionally defined as a transient, reversible, localized disturbance of cerebral blood circulation with complete disappearance of signs and symptoms within 24 hours. With the development of neuroimaging and clinical research, especially the application of ultra-early thrombolytic therapy for ischemic stroke, a new definition is proposed as transient, transient, limited cerebral deficits or retinal dysfunction caused by cerebrovascular lesions, with clinical symptoms lasting no more than 1 hour and no responsible lesions on structural imaging (CT, MRI). The incidence of TIA increases with age, and the incidence of TIA varies widely because of the controversial time limit for TIA episodes. Etiology and pathogenesis The pathogenesis of TIA is related to various etiologies and pathways such as atherosclerosis, arterial stenosis, heart disease, changes in blood composition and hemodynamic changes, and the main pathogenic mechanisms are: 1. Hemodynamic changes The basic etiology may be severe stenosis of arteries in the intracranial arterial system or vertebrobasilar arterial system due to various causes (such as atherosclerosis and arteritis, etc.). When cerebral perfusion decreases (e.g., a drop in blood pressure), the brain area distal to the stenosed artery is transiently ischemic, and local cerebral blood flow returns to normal, TIA symptoms disappear. The clinical symptoms of this type of TIA are relatively stereotypical, with a high frequency of attacks, which can occur several times a day or a week, and the duration of each attack is mostly less than 10 minutes. 2.Microembolism theory Microembolism mainly comes from heart valve cardiogenic embolism, proximal large artery atherosclerotic plaque dislodged, attached wall thrombus dislodged, enter the retina or intracranial blood supply artery through blood flow, blocking the artery leading to ischemia of brain tissue in its blood supply area, causing corresponding symptoms. When the embolus breaks down by the action of enzymes, or when the embolus moves distally due to ischemic dilatation of the vessels distal to the embolus, blood flow is restored and symptoms disappear. There are also some paradoxical emboli, such as those appearing in congenital malformations of the heart with right-to-left shunts, and in TIA of the carotid system, microembolic signals can be detected in the ipsilateral middle cerebral artery with transcranial Doppler. The clinical symptoms of this type of TIA are variable and the episodes are infrequent, occurring once every few weeks or months, and each episode lasts for a long time, up to tens of minutes to 2 hours. 3, vascular spasm, stenosis or compression When vascular spasm occurs in the cerebral vessels by various stimuli, it can cause cerebral ischemic attack. Compression of the vertebral artery by cervical spine osteophytes can cause ischemic attacks in the vertebrobasilar system. 4. subclavian artery steal syndrome When there is subclavian artery stenosis or occlusion, upper limb activity can cause subclavian steal of the vertebral artery and cause TIA of the vertebral basilar artery system. 5. hematological abnormalities (such as true erythrocytosis, thrombocytosis, increased plasma fibrinogen, etc.) Severe anemia and hypercoagulable state due to various causes can also be involved in the development of TIA.