1, pathogenesis and etiology: hemodynamic changes mainly occur on the basis of atherosclerosis or luminal stenosis of the cerebral vascular wall, when blood pressure decreases too much or blood pressure fluctuates significantly, blood flow decreases significantly and the flow rate slows down, causing a sudden decrease in blood flow in the lesioned vessel and triggering a cerebral ischemic event, which is called a hypoperfusion cerebral ischemic event, and improving perfusion can increase the clearance capacity of emboli and avoid stroke This is called hypoperfusion. The regulation of human blood flow is regulated by multiple factors, and the amount of cerebral blood flow is directly related to the mean arterial pressure. The pathogenesis of stroke is broadly divided into cerebral thrombosis, cerebral embolism and systemic hypoperfusion. Blood vessels have the ability to remove emboli, and microemboli can be cleared by fragmentation in blood vessels. It is generally believed that emboli originate from large arteries in the neck and intracranial region, especially from atherosclerotic plaques at arterial bifurcations, attached wall thrombi or microemboli dislodged from the heart, which flow into the brain with blood and can cause occlusion of the corresponding arteries in the skull, producing clinical symptoms. When the microemboli disintegrate or move to the distal end of the vessel, the symptoms disappear when the local blood flow is restored; the inability to disintegrate and move is called embolus clearance disorder. (1) Hemodynamic changes: In elderly patients, hypertension, hyperglycemia, hyperlipidemia and other underlying factors are present, and endothelial cell damage and decreased vascular elasticity can easily lead to cerebrovascular atherosclerosis, narrowing or occlusion of the vascular lumen, and reduced blood perfusion. If there is a sudden drop or fluctuation of blood pressure at this time, it is very easy to lead to the local blood supply of cerebral circulation and ischemic events. (2) Blood rheology changes: patients with underlying disease, vascular endothelial injury, collagen exposure to initiate endothelial repair mechanisms, platelet activation, adhesion and aggregation accelerate thrombus formation; hemodynamic slowing of blood flow is also one of the factors; in addition, the increase in blood viscosity after dehydration and lowering of cranial pressure can promote the formation of cerebral blood flow hypoperfusion. (3) Failure to establish effective collateral circulation: when cerebral blood flow is impaired, good collateral compensation shows unique contribution to ensure brain function, which directly affects the occurrence and regression of the disease. 2, clinical characteristics: the majority of elderly patients, age itself is an independent risk factor for cerebrovascular disease, and most of the patients in this group have a history of hypertension, hyperglycemia and hyperlipidemia, which increases the incidence of cerebral infarction, and some patients have a history of TIA and cerebral infarction, with poor vascular conditions and high requirements for cerebral perfusion pressure and cerebral blood flow supply, in addition, atherosclerosis leads to severe stenosis of large intracranial and extracranial arteries In addition, atherosclerosis leads to severe narrowing and occlusion of large intracranial and extracranial arteries, reduced vascular reserve capacity, poor opening of collateral circulation, sweating, diarrhea, surgery, low water intake, and inappropriate hypotension resulting in reduced effective circulating blood can lead to ischemia and hypoxia in brain tissue in the junctional area of intracranial arteries or other brain tissues, resulting in the occurrence of hypoperfusion-related cerebral ischemic events. The clinical manifestations of patients depend on the degree of hypoperfusion, duration, site and area of cerebral infarction, etc. 3. Prevention and control measures: Neurologists should pay particular attention to the treatment and prevention of this disease, and the key lies in the following points: (1) Firstly, etiological treatment, patients should actively search for the cause and do vascular screening after the occurrence of hypoperfused cerebral infarction. It has been pointed out that most patients with symptomatic hypoperfusion have severe carotid artery stenosis, and carotid endarterectomy or carotid stenting should be considered (2) Active correction of blood pressure status and circulating blood volume deficiency. (3) Dehydration drugs should be used with caution, especially in neurology most of the patients are elderly, and most of them have a history of combined hypertension, diabetes mellitus, coronary artery disease, etc. When there is circulating blood volume plus excessive dehydration or improper drug selection, hypoperfused cerebral infarction is likely to occur; if dehydration drugs must be used pam diuretics should be used with caution and mild dehydration drugs such as glycerol fructose or albumin should be chosen. (3) Oxygen radical scavenging drugs: According to the pathophysiological process of cerebral infarction and the mechanism of damage, the efficacy of this group of patients shows that it has an effective inhibitory effect and scavenging effect on free radical toxic damage. Edaravone, as a representative drug for scavenging oxygen free radicals, can reduce the cascade reaction caused by the toxic effect of free radicals, reduce brain edema and brain damage, delay the time of neuronal death and can significantly improve the neurological function of cerebral infarction. (4) Some of the exacerbations of cerebral infarction patients during hospital treatment are of medical origin and need to be brought to the attention of clinicians to avoid the abuse of drugs with hypotensive effects, such as nimodipine, which can be used as a vascular antispasmodic drug but its hypotensive effect is often the cause of medical origin of cerebral infarction, especially for those admitted with posterior circulation symptoms, and close monitoring of blood pressure changes to ensure cerebral perfusion is a serious and professional issue. (5) Advanced age with carotid atherosclerosis and plaque formation is one of the factors for the occurrence of such cerebral infarction. In conclusion, hypoperfusion of the brain can occur with insufficient blood volume or blood pressure fluctuations, especially when hemodynamic disturbances occur on the basis of large vessel stenosis, further promoting the occurrence of ischemic stroke. The more severe the stenosis, the greater the impact of hypoperfusion has been found in clinical practice. Inadequate perfusion of brain tissue can directly lead to neuronal degeneration, edema and necrosis thus triggering clinical manifestations of neurological deficits. However, the occurrence of cerebral infarction in the presence of hypoperfusion also depends on the establishment of collateral circulation. Therefore, early improvement of perfusion and prevention of hypoperfusion are of great clinical significance to ensure adequate blood supply to the brain and deserve the attention of clinicians.