Cerebral embolism refers to the sudden onset of symptoms of focal neurological deficits such as hemiplegia, hemianesthesia, and slurred speech due to the entry of abnormal solid, liquid, or gaseous objects (called emboli) into the cerebral arterial system along the blood circulation, causing occlusion of the arterial lumen and resulting in necrosis of local brain tissue in the blood supply area of that artery, which clinically manifests as hemiplegia, hemianesthesia, and slurred speech. The disease accounts for 15-20% of cerebrovascular disease. The most common embolus originates from the heart, about 14-48% of rheumatic heart disease patients occur cerebral embolism; myocardial infarction, endocarditis, atrial fibrillation, cardiac surgery is prone to induce this disease; non-cardiac embolus is seen in the carotid atherosclerotic plaque detachment, trauma fracture or pneumothorax, diving or high altitude flight decompression improper, pregnant women giving birth, etc. Clinical manifestations: 1, the onset of the disease is extremely rapid, often in a few seconds or a very short time symptoms reach the peak, a few in a stepwise progressive deterioration. Some patients have transient confusion, headache, and convulsions. Secondary cerebral edema occurring within a few days after larger arterial occlusion can worsen symptoms and lead to impaired consciousness, and severe cerebral edema can also cause the risk of fatal intracranial structural displacement (brain herniation). 3. Sudden onset of neurological focal signs and symptoms. 4.Middle cerebral artery and its deep penetrating branches: most susceptible to involvement, with contralateral hemiparesis (severe degree), hemianesthesia (loss of sensation), ipsilateral hemianopia, and aphasia when the dominant hemisphere (usually the left side) is involved, and aphasia when the non-dominant hemisphere is involved. 5. Internal carotid artery: It can cause ipsilateral blindness, and other symptoms are often difficult to distinguish from those that occur after occlusion of the middle cerebral artery and its deep penetrating branches. 6, anterior cerebral artery: uncommon, one side can cause contralateral hemiparesis, (lower extremity heavy upper extremity light), strong grip reflex and urinary incontinence. Bilateral involvement may cause emotional indifference, blurred consciousness, occasional muteness and spastic paraplegia. 7. Posterior cerebral artery: ipsilateral hemianopia, contralateral hemianesthesia, spontaneous thalamic pain, or sudden involuntary hemianopia; dyslexia can be seen when the dominant hemisphere is involved. 8. Vertebrobasilar artery: vertigo, diplopia, oculomotor paralysis, ataxia, crossed palsy, pupillary abnormalities, tetraplegia, difficulty in eating and swallowing, impaired consciousness, and even death. Diagnosis based on: 1. rapid onset; 2. evidence of embolic origin such as rheumatic heart disease or severe atherosclerosis of the carotid arteries or/and embolism in other parts of the body (retina, kidney, spleen); 3. sudden onset and rapid peak of contralateral hemiparesis (severe degree), hemianesthesia (loss of sensation), isotropic hemianopia, aphasia, aphasia, vertigo, diplopia, oculomotor paralysis, ataxia, crossed paresis, Pupillary abnormalities, tetraplegia, difficulty in eating and swallowing, impaired consciousness and other cerebral artery occlusive syndromes. 4. Positive cranial CT examination or single or multi-site brain tissue hypointensity in accordance with vascular distribution or ischemic or edematous lesions in accordance with vascular distribution on cranial MRI.