Transient ischemic attack (TIA) is a transient deficiency of blood supply in the internal carotid artery system or vertebrobasilar artery system, manifested as a sudden onset of limited neurological deficits, with complete recovery in seconds, minutes and hours, up to 24 hours, without leaving any signs and symptoms, often recurrent. Clinical manifestations of transient ischemic attack (TIA) The disease is more common in men than women after middle age. The onset of TIA is sudden and short-lived, with symptoms and signs peaking rapidly and lasting from seconds to minutes to tens of minutes or hours, with complete recovery within 24 hours without sequelae. The symptoms of focal neurological deficits often appear repeatedly and stereotypically in each patient according to certain areas of vascular innervation, more often than not several times a day, and less often only once in weeks, months or even years. According to the different vessels involved, TIA is clinically classified into two major categories: TIA of the internal carotid artery system and TIA of the vertebrobasilar artery system. (a) TIA of the internal carotid artery system has various symptoms, with TIA of the innominate area of the middle cerebral artery being the most common. Common symptoms may include weakness, numbness, sensory loss or loss of the lateral upper and/or lower extremities, and also aphasia, dyslexia, dyscalculia, and dysgraphia; hemianopia is less common, and paralysis is usually more severe in the upper extremities and face. Transient monocular blindness is a characteristic symptom of ischemia in the internal carotid artery, which is unique to TIA of the internal carotid system. If the episodic hemiparesis is accompanied by transient monocular blindness or visual disturbance on the contralateral side of the paresis, the clinical diagnosis is a transient ischemic attack of the internal carotid artery on the side of blindness. The above symptoms may occur separately or in combination. (ii) TIA of the vertebrobasilar system sometimes presents only with vague symptoms such as dizziness, blurred vision, and unsteady walking, making it difficult to diagnose. Focal symptoms are most commonly vertigo, which is usually not accompanied by significant tinnitus. If there are symptoms of brainstem and cerebellar involvement such as diplopia, dysarthria, dysphagia, crossed or bilateral limb paresis and other sensory disorders, ataxia, the diagnosis is clearer. Insufficient blood supply to the posterior cerebral artery may manifest as cortical blindness and visual field defects. The patient suddenly loses tension in both lower limbs and falls to the ground without any perceptible impairment of consciousness, and the patient can stand up immediately, which is caused by bilateral brainstem reticular ischemia. Posterior occipital headache and sudden collapse, especially after rapid head or upper extremity movement, may indicate inadequate blood supply to the vertebrobasilar system and the possibility of cervical spondylosis and subclavian artery steal. Some symptoms can be seen in both the internal carotid artery system and the vertebrobasilar system. These symptoms include dysarthria and isotropic hemianopia. In cases of vertigo (with or without nausea or vomiting), dysarthria, dysphagia and diplopia, the diagnosis of TIA should not be made easily, but should be combined with other clinical tests to find the exact cause. A combination of 2 or more of these symptoms, or crossed paralysis with motor, sensory, and visual disturbances and ataxia, is diagnosed as a vertebrobasilar TIA episode. The time frame of TIA is brief, lasting less than 15 minutes, usually no more than 30 minutes, and rarely up to 12-24 hours. However, if neurological signs can still be detected after 24 hours, it is clearly a cerebral infarction. The course and prognosis of transient ischemic attack: The natural history of TIA is 25-40% of cerebral infarction within 5 years, and many retrospective prospective studies have confirmed the severity of TIA. TIA is a precursor of severe ischemic cerebrovascular disease, especially when TIA attacks are frequent in the carotid system, the possibility of cerebral infarction is greater. Cerebral infarction occurs within 1 month of TIA onset in about 36% of patients and within 12 months in 50%. It is estimated that about 1/3 of TIA episodes continue without lasting dysfunction, 1/3 experience cerebral infarction, and the other 1/3 stop on their own. According to many years of clinical reports, TIA is not only a precursor to cerebral infarction but also to myocardial infarction, and myocardial infarction is often the main cause of death in TIA patients. Therefore, TIA attacks should be treated as an emergency.