Cerebral infarction is the necrosis of local brain tissue including nerve cells, glial cells and blood vessels due to lack of blood supply. The underlying cause of cerebral infarction is the failure to obtain timely and adequate collateral circulation due to occlusive lesions in the extracranial or intracranial arteries supplying blood to the brain, resulting in an oversupply phenomenon between the metabolic needs of local brain tissue and the possible blood supply beyond a certain limit. The causes of blood supply disorders are the following three aspects. 1, vascular lesions the most important and common vascular lesions are atherosclerosis and thrombosis occurring on this basis. This is followed by small cerebral arteriosclerosis associated with hypertensive disease. Others are normal vascular development, such as congenital aneurysm and cerebrovascular malformation can occur thrombosis, or bleeding resulting in impaired blood supply to adjacent areas; vasculitis, such as infectious rheumatic fever, tuberculosis and endarteritis due to syphilis, which has been extremely rare in China. 2, the change of blood components vascular lesions at the endothelium rough, so that the blood platelets easy to attach, accumulate and release more pentothal and other chemicals; blood components in lipoprotein, cholesterol, fibrinogen and other content of the increase in blood viscosity and red blood cell surface negative charge, resulting in slowing down the blood flow; and blood diseases such as leukemia, erythrocytosis, severe anemia, and a variety of The factors that affect the increase of blood coagulability make thrombosis easy to occur. 3, blood flow changes in the regulation of cerebral blood flow, by a variety of factors. The change of blood pressure is an important factor affecting the local blood flow. When the average arterial pressure is lower than 9.3kPa (70mmHg) and higher than 24kPa (180mmHg), the blood supply to local brain tissue is about to be impaired due to the lesion of blood vessel itself, the narrowing of blood vessel and the failure of auto-regulation function. Some systemic diseases such as hypertension and diabetes mellitus can accelerate or aggravate cerebral atherosclerosis, which is also closely related to the occurrence of cerebral infarction. Most of the patients who are usually clinically diagnosed with cerebral infarction or cerebral thrombosis are atherosclerotic thrombotic cerebral infarction, referred to as atherosclerotic cerebral infarction. In addition, another important cause of cerebral infarction is the embolism of cerebral arteries, namely cerebral artery embolic cerebral infarction, referred to as cerebral embolism. A. Atherosclerotic cerebral infarction Atherosclerotic thrombotic cerebral infarction, referred to as atherosclerotic cerebral infarction, is a local brain tissue necrosis caused by atherosclerosis and thrombosis in the arterial system supplying the brain, resulting in acute cerebral blood supply deficiency, which is often clinically manifested as sudden focal neurological deficits such as hemiplegia and aphasia. The old name is cerebral thrombosis. The underlying cause of atherosclerotic cerebral infarction is atherosclerosis. The most common co-morbidity is hypertension. Although there is no direct etiologic link between the two, hypertension often accelerates and exacerbates the development of atherosclerosis. Atherosclerosis is a non-inflammatory lesion that can occur in arterial walls throughout the body. Its pathogenesis is related to impaired lipid metabolism and endocrine alterations, the exact cause of which has not been elucidated. The main changes are fatty degeneration and cholesterol deposition in the deep intima of the arteries, forming atherosclerotic plaques and various secondary lesions, resulting in lumen narrowing or even occlusion. The narrowing of the lumen needs to reach 80-90% before it affects cerebral blood flow. The sclerotic plaque itself does not cause symptoms. As the lesion progresses, the intima splits, subintimal hemorrhage (caused by rupture of a nutrient vessel in the artery itself) and an intimal ulcer develops. The intimal ulcer is prone to thrombosis, which further narrows or occludes the lumen; the contents of the sclerotic plaque or debris from the thrombus may dislodge into the bloodstream to form an embolus. Clinical manifestations of atherosclerotic cerebral infarction: atherosclerotic development of cerebral arteries, generally 10 years later in age than the same degree of coronary atherosclerosis. the incidence of atherosclerotic cerebral infarction increases after the age of 60. It is slightly more common in men than in women. High fat dieters with high blood cholesterol and low HDL cholesterol are prone to atherosclerosis formation. Other conditions such as hypertension, diabetes mellitus, smoking, and erythrocytosis have a higher incidence. Atherosclerotic cerebral infarction accounts for about 60-80% of strokes. The onset of the disease is slightly slower than other strokes, often peaking in minutes to hours, half a day, or even a day or two. Gradual worsening to a peak within a few days to a week is extremely rare. Many patients have a stroke during sleep. About half of the patients have experienced a transient ischemic attack in the past. Mild headache may be present at the onset, probably due to compensatory vasodilatation of the collateral circulation. The headache is often predominant on the ischemic side of the head and may sometimes be accompanied by pain behind the eyes. Hemiparesis in atherosclerotic cerebral infarction often occurs with clear consciousness. If unconsciousness is present at the onset of the disease, consider cerebral infarction of the vertebrobasilar system. Infarction, ischemia, and edema in larger areas of the cerebral hemispheres may affect the function of the mesencephalon and upper brainstem, and impairment of consciousness may occur shortly after the onset of the disease. Symptoms of focal damage to the brain depend mainly on the distribution of the involved vessels. For example, the clinical manifestations of atherosclerotic cerebral infarction in the carotid system are mainly paralysis or sensory impairment of the limb contralateral to the lesion; lesions in the dominant hemisphere are often accompanied by varying degrees of aphasia, and lesions in the non-dominant hemisphere are accompanied by hemiplegic agnosia. The patient’s two eyes gaze toward the side of the lesion. If there is blindness in one eye on the focal side with motor or sensory deficits in the contralateral limb, there is no doubt that the lesion is an internal carotid artery lesion. Stenosis or occlusion of the internal carotid artery can cause severe symptoms due to ischemia of the entire cerebral hemisphere, or it can manifest only trivial symptoms. This highly variable condition depends on the compensatory function of the anterior and posterior communicating arteries, ophthalmic artery, superficial cerebral artery and other collateral circuits. If paralysis and sensory disturbances are limited to the face and upper extremities, ischemia in the area supplied by the middle cerebral artery is more likely. Cerebral infarction of the anterior cerebral artery may cause paralysis of the contralateral lower extremity, but this paralysis may not occur due to the supply of the anterior cerebral communicating artery by the collateral circulation. The posterior cerebral artery supplies the posterior part of the cerebral hemispheres, the thalamus, and the superior brainstem, and cerebral infarction may result in contralateral isotropic hemianopia. In addition to cortical sensory deficits, aphasia, dyslexia, dyscalculia, and parietal syndrome may occur if the lesion is in the main hemisphere. The main manifestations of atherosclerotic cerebral infarction of the vertebrobasilar system are vertigo, nystagmus, diplopia, isotropic hemianopia, cortical blindness, oculomotor paralysis, dysphonia, dysphagia, limb ataxia, crossed paralysis or sensory impairment, and tetraplegia. There may be posterior-occipital headache and varying degrees of impaired consciousness. Prevention and treatment of atherosclerotic cerebral infarction Atherosclerosis patients should consume a low-fat diet with more vegetables and vegetable oils, and less cholesterol-rich foods, animal offal, egg yolk and animal oil. In case of hypertension and diabetes, attention should be paid to the treatment of the disease. Pay attention to prevent conditions that may cause sudden drop in blood pressure, such as overdose of antihypertensive drugs, severe diarrhea, hemorrhage, etc. Have a regular life. Pay attention to the combination of work and rest, avoid overexertion of body and mind. Perform appropriate health care gymnastics regularly to strengthen cardiovascular stress capacity. For those who have transient cerebral ischemic attack, they should be treated actively. This is an important link to prevent the occurrence of atherosclerotic cerebral infarction. Cerebral embolism is also known as ischemic stroke when an abnormal object (solid, liquid, gas) enters the cerebral artery or the carotid artery supplying the brain along the blood circulation, causing blood flow obstruction and resulting in cerebral infarction. Cerebral embolism accounts for 10-15% of the incidence of stroke, and 2/3 of recurrences occur within 1 year of the first onset. The etiology of cerebral embolism: the source of emboli in cerebral embolism can be divided into three categories: cardiogenic, non-cardiogenic, and of unknown origin. Clinical manifestations of cerebral embolism: The age of onset of cerebral embolism varies. Most of them are related to heart disease, especially rheumatic heart disease, so the age of onset is mostly young and middle-aged. The onset of the disease is extremely rapid, and most of them do not have any prodromal symptoms. Symptoms often peak within seconds or a short time after onset. The cerebral embolism may occur in a single artery or may be widespread, so that the clinical manifestations vary. Except for internal carotid artery embolism, patients are usually not comatose. Some patients may experience transient confusion, headache, or convulsions at the onset of the disease. Focal neurological symptoms occur suddenly and are limited to the distribution of one arterial branch. The clinical manifestations are facial paresis, upper extremity monoparesis, hemiparesis, aphasia, focal convulsions, and other manifestations of internal carotid artery-middle cerebral artery system lesions because embolism occurs in the anterior half of the distribution of the fundic artery ring in about 4/5 of cases. Hemiparesis is also more severe in the face and upper extremities and relatively mild in the lower extremities. Sensation and vision may be mildly affected. However, they are usually not significant. Most of the convulsions are limited, but if they are generalized grand mal seizures, the infarction is widespread and severe. 1/5 of cerebral embolisms occur in the distribution area of the posterior half of the arterial ring at the base of the brain and may present with vertigo, diplopia, ataxia, crossed paralysis and other manifestations of vertebrobasilar artery system lesions. Treatment of cerebral embolism: Prevention and treatment of heart disease is an important part of prevention and treatment of cerebral embolism. Once cerebral embolism occurs, the treatment is in principle the same as that for atherosclerotic cerebral infarction. The patient should be placed in the left lateral position. Dextran 40, vasodilator drugs and hormones all have certain effects. Since the congestive infarct area of cardiogenic cerebral embolism such as rheumatic mitral valve lesion is extremely prone to bleeding, anticoagulation therapy must be used with caution.