Prevention and treatment of cerebral infarction According to the book “Prevention and treatment guide of cerebrovascular disease in China”, it is expected that by 2030, the population over 60 years old in China will reach more than 300 million, and about 2/3 of the people with the first onset of cerebrovascular disease are the elderly population over 60 years old. In recent years, due to unreasonable personal habits or environmental factors of personal life, the age of cerebrovascular first attackers is gradually getting younger. In China, every 12 seconds there will be 1 new onset of cerebrovascular disease, and every 21 seconds there will be 1 death from cerebrovascular disease. According to experts, cerebrovascular disease has now become the first disability and the second most deadly disease in China. According to the statistics of the Ministry of Health, there are 2.5 million new cases of cerebrovascular disease in China every year, and as many as 1.5 million people die from cerebrovascular disease every year, of which about 60% – 80% are patients with cerebral infarction. In addition, among the surviving cerebrovascular disease patients, it is very easy to have another or multiple attacks, and about three quarters of them are incapacitated to varying degrees, among which 40% are severely disabled. Because of the high cost of cerebrovascular disease treatment, it has caused a heavy burden to many patients and families psychologically and economically. Cerebral infarction, also known as ischemic stroke, refers to ischemic necrosis or cerebral softening of restricted tissues caused by ischemia and hypoxia due to impaired blood supply to the brain. The common clinical types of cerebral infarction include cerebral thrombosis, lacunar cerebral infarction and cerebral embolism. 1. Atherosclerosis Atherosclerotic thrombosis (cerebral thrombosis): Atherosclerotic thrombosis is the most common type of cerebral infarction. Patients of advanced age, with a history of hypertension, diabetes mellitus, hyperlipidemia, etc., especially with a history of myocardial ischemia, all suggest the possibility of atherosclerosis. Atherosclerosis usually refers to the narrowing or occlusion of the lumen of cerebral arteries or their cortical branches due to atherosclerosis, which leads to thrombosis, resulting in interruption of blood flow to the local blood supply area of the brain, ischemia, hypoxia, softening and necrosis of brain tissue, and the appearance of corresponding neurological symptoms and signs. Atherosclerosis is the basic cause of the disease, leading to atherosclerotic cerebral infarction, often accompanied by hypertensive disease, and atherosclerosis as a cause and effect, diabetes mellitus and hyperlipidemia can also accelerate the process of atherosclerosis. Cerebral atherosclerosis mainly occurs in large arteries with a diameter of 500 μm or more. Atherosclerotic plaques lead to luminal narrowing and thrombosis, which can be seen anywhere in the internal carotid artery and vertebrobasilar artery system, mostly at arterial bifurcations, such as the bifurcation of the common carotid artery with the internal and external carotid arteries, the beginning of the anterior and middle cerebral arteries, the beginning of the vertebral artery in the subclavian artery, the vertebral artery into the intracranial segment, and the beginning and bifurcation of the basilar artery. Artery-artery embolism: In addition, atherosclerosis of large arteries can lead not only to cerebral thrombosis but also to artery-artery embolism. Watershed cerebral infarction: cerebral watershed infarction caused by large cerebral artery stenosis combined with low perfusion or impaired removal of microemboli accounts for approximately 10% of cerebral infarction, and these patients generally have better treatment results. 2.Lacunar cerebral infarction (small vessel lesion): lacunar cerebral infarction refers to ischemic microinfarction occurring in the deep white matter of the cerebral hemispheres and brainstem, due to ischemia, necrosis, liquefaction of brain tissue and removal by phagocytes to form lacunae, accounting for about 20% of cerebral infarction. Etiology and pathogenesis: (1) Hypertension causes lipid hyaline degeneration in the walls of small arteries and tiny arteries, resulting in luminal occlusion and lacunar lesions. (2) Atherosclerotic lesions in the middle cerebral artery and basilar artery and the formation of small thrombi can involve and obstruct the deep penetrating arteries and lead to lacunar infarction. (3) Atherosclerosis of deep penetrating branch arteries. 3, cerebral embolism Cerebral embolism refers to the acute occlusion of vascular lumen caused by various emboli entering the intracranial arterial system with blood flow, resulting in ischemic necrosis and brain dysfunction of brain tissue in the corresponding blood supply area. Etiology: Cerebral embolism can be classified according to the different sources of emboli: (1) cardiac: the most common, accounting for 60%-75% of cerebral embolism, cerebral embolism is usually one of the important manifestations of heart disease, the most common direct cause is chronic atrial fibrillation. (2) Non-cardiac origin: such as dislodgement of atherosclerotic plaque, pulmonary vein thrombosis or blood clot, fat embolism and air embolism during fracture or surgery, etc. (3) Unknown origin: About 30% of cerebral embolism cannot be identified as the cause. Cardiogenic embolism mostly occurs in patients with heart disease, such as rheumatic heart disease and atherosclerotic heart disease, with atrial fibrillation causes more than half of them, subacute bacterial endocarditis redundant on the valve, myocardial infarction or cardiomyopathy attached to the wall thrombus, mitral office prolapse, cardiac mucinous tumor and cardiac surgical comorbidity, etc., also often cause cerebral embolism, congenital heart disease atrioventricular septal defect In the case of congenital heart disease, emboli from the venous system of body circulation, when the right intracardiac pressure is greater than the left intracardiac pressure, can enter the intracranial artery directly without passing through the pulmonary circulation and cause cerebral embolism, which is called paradoxical embolism. Cardiogenic cerebral embolism starts rapidly, its cerebral infarct volume is larger, neurological function damage is usually heavy, and the prognosis is relatively poor. In recent years, syphilitic vasculitis and infectious vasculitis caused by AIDS have a rising trend and should be paid attention to, in addition, systemic lupus erythematosus can lead to central nervous system vasculitis, giant cell arteritis and multinodular arteritis can also be seen; erythrocytosis and thrombocytosis, hypercoagulable state is not uncommon; smog disease can lead to central nervous system vasculitis, giant cell arteritis and multinodular arteritis. Erythrocytosis and thrombocytosis, hypercoagulability are not uncommon; smog can lead to many types of cerebral infarction; drug abuse such as cocaine and heroin can also lead to cerebrovascular lesions. Other rare causes include hyperfibrinogenemia, antithrombin III deficiency, protein S and C deficiency, pregnancy, tumors, anticardiolipin antibody syndrome, and sickle cell disease. Among the genetic vascular diseases, CADASIA is currently clear. Treatment Staging of cerebral infarction: The pathophysiological and biochemical changes of ischemic brain damage show a dynamic development process, and a typical cerebral infarction can basically be clinically divided into several stages, namely the acute phase (1 month), the recovery phase (2-6 months), and the sequelae phase (after 6 months). Focusing on the treatment of the acute phase, lacunar cerebral infarction should not be dehydrated, mainly to improve circulation; large and medium infarcts should be actively anti-cerebral edema to lower cranial pressure and prevent brain herniation formation.