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Mechanism of brain function damage caused by cerebrovascular disease ?

How is brain function damaged after cerebrovascular disease ? At present, there are mainly the following aspects : 

1 energy failure : cerebral thrombosis or cerebral embolism blocked the distal vascular lesions of the blood supply, vascular lesions dominated by the region of neurons due to reduced blood supply, nutrient and energy supply is insufficient, the neurons themselves stored very limited energy quickly exhausted, neurons can not complete the normal physiological function, the occurrence of acute degeneration and necrosis. In cerebral hemorrhage, blood flow to the distal end of the ruptured vessel is reduced or completely stopped, resulting in a lack of brain tissue energy in the vascular territory. 

2.Secondary injury after ischemia : Ischemic neurons can not maintain normal metabolic function. Excitatory amino acids with neurotoxicity are released to the outside of cells in large quantities. Calcium ions are influxed in large quantities and oxygen free radicals are generated, which further damage brain cells, aggravate necrosis of neurons in the ischemic area and induce apoptosis of neurons in the ischemic peripheral area. 

3. Brain edema : Brain edema refers to excessive water content in brain tissue. According to different causes, brain edema can be divided into three types. The first is cytotoxic brain edema, it is due to brain cells ( including neurons and glial cells ' energy metabolism disorder after ischemia, can not maintain the balance of intracellular and extracellular ions, extracellular sodium ions and water into a large number of cells, brain cell swelling and brain edema. The second is vasogenic brain edema, which is due to cerebral ischemia, cerebrovascular energy supply shortage, vascular endothelial cell swelling, damage, increased vascular permeability, blood-brain barrier damage. Components in the plasma seep into the brain tissue to cause brain edema. The third is interstitial brain edema, caused by subarachnoid hemorrhage, cerebral hemorrhage, large area of cerebral infarction caused by increased cerebrospinal fluid pressure, cerebrospinal fluid into the brain tissue gap and lead to brain edema. On the one hand, brain edema affects the material and energy exchange between brain cells and the outside world. On the other hand, it compresses blood vessels and further reduces blood flow. More seriously, local brain edema can make brain tissue shift ( medically called brain disease ) and endanger life. This is why acute cerebrovascular disease requires dehydration therapy.

4. Occupying effect : cerebral hemorrhage hematoma and severe local brain edema compression lesions around the brain tissue, resulting in occupying effect. The sudden occupying effect can reduce the blood supply of the surrounding brain tissue, compress the nerve fibers to break, and destroy the normal nerve conduction function. Another sub-heavy consequence of the placeholder effect is brain defects that threaten the lives of patients. Occupying effects in the cerebellum tend to compress the life center in the brainstem. So, even if not too big cerebellar hemorrhage, can also lead to patient ' lightning ' death. 

5.Cerebral vasospasm : mostly occurs in subarachnoid hemorrhage. Because the whole brain tissue is immersed in bloody cerebrospinal fluid, red blood cells and a large number of vasoconstrictors produced by their decomposition stimulate the blood vessels on the surface of the brain, causing widespread and persistent cerebral vasospasm, extensive ischemia of brain tissue, and secondary cerebral infarction in sub-severe cases. So subarachnoid hemorrhage generally need anti vasospasm treatment. In addition, cerebral embolism can also cause reflex spasm of adjacent cerebral vessels and aggravate ischemic damage. Younger patients have higher vascular reactivity and cerebral vasospasm is often more severe.

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