Cerebral infarction is the pathological name for the softening and necrosis of brain tissue caused by ischemia and hypoxia due to an obstacle in the blood supply to the brain. The acute phase of cerebral infarction refers to the period from the onset of the disease to two weeks after the disease. Pathology and physiology of acute cerebral infarction: The purpose of understanding the pathology and physiology of cerebral infarction is to guide clinical treatment. The occurrence of cerebral infarction depends on the paradoxical pair of blood vessel walls and blood components. The most common cause of cerebral infarction is atherosclerosis. Atherosclerosis causes narrowing of the lumen, and when the narrowing is more than 80%, the cerebral blood flow decreases. Some experiments showed that when the local cerebral blood flow decreased to 5ml/100mg/min, somatosensory evoked potentials disappeared, but there was no change in extracellular K activity; at this time, the neuronal damage was reversible. When the local cerebral blood flow decreased to 6 ml/100 mg/min, the extracellular K activity suddenly increased, and the structural damage was irreversible. This suggests the necessity and importance of early clinical treatment of ischemic infarction. Causes of cerebral infarction most scholars believe that arterial-arterial embolism has the most chances, embolism mostly comes from sclerotic plaque or broken microembolism in the wall of the large arteries, in addition to the redundancy in the heart, and a few are thrombosis. Acute cerebral infarction causes: 1, vascular lesion factors: hypertension caused by arterial spasm, atherosclerosis plaque formation, diabetic vascular lesions and arterial inflammation. 2.Blood component factors: high coagulation state of blood – platelet increase, fibrinogen increase, blood viscosity increase and so on. Mechanical factors: arterial embolism, mostly from the heart and large blood vessels; fat and other embolisms caused by trauma; traumatic vascular occlusion and so on. 4, blood perfusion factors: can be seen in chronic hypotension caused by watershed cerebral infarction, cerebral white matter ischemia. Different cerebral infarction patients, leading to different causes of the disease, different causes should choose different treatment methods, so make a diagnosis must actively look for the cause of the disease. (1) According to the medical history, vascular examination and cardio-encephalographic examination, determine whether there is a possible source of cardiac embolism and evidence of carotid artery stenosis. (2) Look for risk factors, mainly hypertension, diabetes mellitus, increased erythrocyte pressure volume, hypercoagulability and hyperlipidemia. Diagnosis of acute cerebral infarction: Clinical manifestations: the onset of disease is rapid, in a few seconds to a few hours of the brain focal symptoms and signs of hemiparesis, aphasia, etc. should be highly suspicious of the possibility of cerebral infarction, cerebral infarction focal symptoms are also divided into the internal carotid artery system and the vertebral basilar artery system, the cerebral infarction is more often in the onset of a relatively quiet, early onset of no headache, vomiting, and impaired consciousness, cerebrospinal fluid examination The cerebrospinal fluid is clear and transparent. The first choice of examination in the diagnosis of cerebral infarction should be cranial CT. CT examination can immediately distinguish between cerebral hemorrhage or cerebral infarction, and CT examination of the brain can also distinguish between non-stroke diseases such as brain tumors. Generally, the diagnosis of cerebral infarction is made by CT scanning without the use of intensifier. On CT, infarcts are typically characterized by low-density foci, but it takes more than 24 hours from the onset of symptoms for most of these foci to appear. The earlier the appearance of hypointense lesions, the more severe the disease, the worse the prognosis, and the more likely to have post-infarction hemorrhage. Regardless of whether there is a positive finding on CT brain, as long as there is no sign of hemorrhage, the presence of neurological deficit symptoms and signs should be treated as cerebral infarction. If the lesion is too small or if there is a suspicion of infarction in the posterior cranial recess, which is difficult to be visualized by CT, then MRI can be considered. In addition, auxiliary tests should be done (1) electrocardiogram and X-ray examination except heart disease; (2) blood cell and platelet count, prothrombin time, etc.; (3) blood electrolytes, blood glucose, liver and kidney function tests, suspected of hypoxemia, blood gas analysis; (4) generally do not do lumbar puncture examination, but suspected of subarachnoid hemorrhage and CT negative or suspected of intracranial infections, do the cerebrospinal fluid examination; (5) suspected of subarachnoid hemorrhage, but the cerebral spinal fluid examination; (6) suspected of subacute hemorrhage, but the cerebral spinal fluid examination; (7) suspected of subacute hemorrhage, but CT negative or intracranial infections; (8) suspected of cerebral infarction. (5) Electroencephalography can be done when epilepsy is suspected. Differential diagnosis: The difference between cerebral infarction and cerebral hemorrhage is that cerebral hemorrhage is often onset in the dynamic, and accompanied by headache, vomiting, impaired consciousness, bloody cerebrospinal fluid and so on. Before diagnosis, non-stroke diseases such as brain tumor should be excluded. Syncope. Epilepsy, etc. However, with the continuous development of examination methods, the previous neurological diagnostic principle of localization before characterization has been replaced by CT or MRI of the brain. If CT examination is not available in rural areas, clinicians still need to follow the diagnostic steps of localization before characterization to avoid delay in diagnosis.