Basic etiology

Atherosclerosis is the basic cause of the disease, leading to atherosclerotic cerebral infarction, often accompanied by hypertension, and atherosclerosis as a cause and effect of each other, diabetes mellitus and hyperlipidemia can also accelerate the process of atherosclerosis. Cerebral atherosclerosis mainly occurs in the tube 500μm above the large arteries.

Atherosclerotic plaques lead to luminal narrowing and thrombosis can be seen in the internal carotid artery and vertebral - basilar artery system in any part of the arterial bifurcation, mostly in the arterial bifurcation, such as the common carotid artery and internal and external carotid artery bifurcation of anterior and middle cerebral arteries in the beginning of the vertebral artery in the subclavian artery in the beginning, the vertebral artery into the intracranial segment of the basilar artery in the beginning of the bifurcation and the bifurcation.

2.? Other etiologies

In addition, it also includes arteritis (such as connective tissue disease and bacterial viral spirochete infections, etc.) and pharmacogenetic (such as cocaine amphetamine) caused. Erythrocytosis thrombocytosis, thromboembolic thrombocytopenic purpura, diffuse intravascular coagulation, sickle cell anemia and other hematologic disorders caused by rare; cerebral amyloid angiopathy Moyamoya disease, myofibrillar dysplasia, and intracranial and extracranial (carotid, intracranial, and vertebral) entrapment aneurysms, etc. Rare.

Some cases of cerebral infarction, although confirmed by imaging, but it is difficult to find the exact cause, the possible causes include cerebral vasospasm, microemboli of unknown origin, antiphospholipid antibody syndrome protein C and protein S abnormalities, antithrombin III deficiency, incomplete release of fibrinogen activator with hypercoagulable state.

3.? Pathogenesis

Atherosclerosis of the cerebral artery trunk or cortical branch arteries caused by various etiological factors, which in turn leads to intima-media thickening lumen stenosis and occlusion and thrombosis, and a sudden reduction or cessation of blood flow in the arteries supplying blood to the brain tissue causing ischemia and hypoxia of the brain tissue of the blood-supplying area of the blood vessel, resulting in brain necrosis, softness, and cerebral thrombosis and accompanied by the corresponding parts of the clinical signs and symptoms, such as hemiplegia aphasia, etc. The incidence of cerebral infarction is also very high. The incidence of cerebral infarction in the internal carotid artery system accounts for about 4/5 of the vertebral-basilar artery system is about 1/5 of the occluded blood vessels, in order of the internal carotid artery middle cerebral artery posterior cerebral artery, cerebral anterior cerebral artery and vertebral-basilar artery and so on. Atherosclerosis or vasculitis can be seen in the occluded vessels altering thrombosis or emboli. Cerebral ischemia generally forms white infarction infarction area brain tissue softening, necrosis with cerebral edema and pericapillary punctate hemorrhage large cerebral infarction can occur hemorrhagic infarction. Ischemic-hypoxic damage can occur in both necrosis and apoptosis of nerve cells.

4. Pathological staging of cerebral ischemic lesions

(1) Ultra-early stage (1-6h): the lesion is not obvious changes in the brain tissue can be seen in some of the vascular endothelial cells, neuronal cells, and astrocytes are swollen mitochondria are swollen and vacuolated.

(2) Acute phase (6～24h): ischemic area brain tissue pale and mild swelling, neuronal cells glial cells and endothelial cells were obvious ischemic changes.

(3) Necrotic phase (24～48h): a large number of neuronal cells disappeared, glial cells were necrotic, neutrophils, lymphocytes and macrophages infiltrated, and the brain tissue was obviously edematous.

(4) Softening phase (3 days to 3 weeks): the lesion area liquefies and becomes soft.

(5) Recovery period (after 3 to 4 weeks): liquefied necrotic brain tissue is cleared by the lattice cells, the brain tissue atrophies, and the small lesions form a glial scar large lesions form a stroke capsule, and this period lasts for several months to 2 years.

5. Pathophysiology

PathophysiologyThe brain tissue is very sensitive to ischemia and hypoxia damage, cerebral artery occlusion leads to ischemia for more than 5min can occur cerebral infarction after ischemic neuronal injury with selective mild ischemia only some neurons are lost in complete and persistent ischemia ischemia ischemic area of all kinds of neurons, glia, and endothelial cells are necrotic.

(1) The central necrotic area and the surrounding ischemic penumbra (ischemic penumbra) are composed of: the necrotic area due to complete ischemia leads to the death of brain cells, but the ischemic penumbra still exists in the collateral circulation, which can obtain part of the blood supply, and a large number of neurons are still viable. If the blood flow is restored quickly so that the brain metabolism improves, the damage is still reversible, the neuronal cells are still viable and restore Function. Therefore, the protection of these reversibly damaged neurons is the key to the treatment of acute cerebral infarction.

(2)Reperfusiondamage: Studies have confirmed that the time window for ultra-early treatment of cerebral ischemia is within 6h, and if cerebral blood flow recirculation exceeds this time window, brain damage can continue to intensify, resulting in reperfusiondamage.

Currently, it is believed that the mechanism of reperfusion injury mainly includes: excessive formation of free radicals (freeradical) and free radicals "waterfall" chain reaction of intracellular calcium overload in neuronal cells, excitatory amino acid cytotoxicity, and a series of changes such as acidosis, which leads to neuronal cell injury.

The concept of ischemic semi-dark band and reperfusion injury has updated the concept of clinical treatment of acute cerebral infarction, and the key to rescue the ischemic semi-dark band is ultra-early thrombolytic therapy to reduce the reperfusion injury, the core of which is to actively take brain protection measures.