Through a large number of clinical and pathological observations, most scholars now believe that cerebral hemorrhage is not caused by a single factor, but may be the result of several combined factors. Elevated blood pressure alone is not sufficient to cause cerebral hemorrhage. Cerebral hemorrhage mostly occurs on the basis of hypertension and chronic arterial lesions caused by hypertension, and the following factors may be related to cerebral hemorrhage. (a) Microaneurysm formation and rupture Microaneurysm, also known as miliary aneurysm, whose formation and rupture lead to hypertensive cerebral hemorrhage is currently recognized as the main pathogenesis. As early as 1868, Charcot-Bouchard studied the brains of people who died of cerebral hemorrhage and found that microaneurysms existed in the small cerebral arteries of hypertensive patients, and these aneurysms were between 0.2 and 1.0 mm in size, often located at the bifurcation of small arteries, almost always multiple and visible to the naked eye. In 1967, Cole and Yates examined and compared the brains of 100 autopsy patients each with hypertension and normal blood pressure and found that 46 cases in the hypertensive group had cornu-like microaneurysms, of which the incidence of cerebral hemorrhage was 86%, while only 7 cases in the normal blood pressure group microaneurysms were found. These microaneurysms are the result of damage to small cerebral arteries caused by hypertension, and they are mostly found in gray matter structures, especially in brain regions such as the nucleus accumbens, pallidum, thalamus, pons, and dentate nucleus, which are consistent with the prevalence of cerebral hemorrhage in hypertension. Due to the sclerosis and hyaline degeneration of small arteries, the elasticity of the vessel wall is lost, the strength is reduced, the vessel wall expands at local weaknesses, lacks the normal hierarchical structure of the vessel wall, cannot contract, lacks self-protection, and is prone to rupture and bleeding when the blood pressure is further increased. (B) Bleeding from damaged small artery walls The cerebral arteries of hypertensive patients, both the internal carotid artery and the vertebrobasilar artery system, are more commonly and severely atherosclerotic than those with normal blood pressure. It has been shown that long-term hypertension has a damaging effect on the intima and walls of the 100-1300 μm diameter penetrating arteries in the cerebral ventricular mass. This is especially true for the ductus arteriosus, which emanates from the anterior and middle cerebral arteries, and the thalamus, which emanates from the basilar artery. Because these arteries are direct terminal arteries from the great arteries, they are not subjected to the same gradual decay of transmural pressure as the small cortical arteries. In the early stages, small arteries show spastic changes; in the middle and late stages, small artery walls show degenerative changes; lipids in the plasma pass through the damaged intima into the subintima, increasing the permeability of the intima, and other components such as plasma and fat accumulate in the vessel wall, forming lipohyalinosis, fibrinoid necrosis In 1983, Takabayashi et al. examined arteries with cerebral hemorrhage and confirmed that the ruptured vessels were at or near the bifurcation of the arteries, and most of these small arteries could be seen with elastic plate dissection, mid-layer fibrosis and intimal thickening, and replacement of smooth muscle with fibrous or necrotic tissue. They are prone to rupture and bleed when there is a rapid change in blood pressure or blood flow. (C) cerebral amyloid angiopathy (amyloid angiopathy) is a lesion that occurs selectively in the cerebral vasculature, mainly invading the soft meningeal arteries and cortical arteries of the brain, and can spread to the small arteries of the brain parenchyma, with amyloid deposits in the middle and outer membranes of the affected vessels, resulting in amyloid degeneration of the walls of the small arteries in the brain, causing the affected arteries to lose their contractile function, and in When hemodynamic changes occur, rupture and bleeding are likely to occur. The hematoma occurs in the peripheral areas of the cerebral hemispheres such as the occipital, temporal and frontal lobes, but not in the basal ganglia, cerebellum and brainstem. It often presents as multifocal, recurrent cerebral hemorrhage, and the hemorrhage volume is often large. The hematoma may also break through the cortex into the subarachnoid space or lateral ventricles. It is generally believed that cerebral amyloid angiopathy is not significantly related to hypertension, but it can coexist with hypertensive disease, and care should be taken to differentiate it. (iv) Bleeding after cerebral softening Embolization of cerebral arteries caused by spasm of small arteries and detachment of atherosclerotic plaques due to hypertension can lead to ischemic softening of brain tissue and secondary necrosis of cerebral vessel walls, resulting in bleeding with weakened perivascular support. (E) The outer membrane and middle layer of cerebral arteries are structurally weak The middle cerebral artery is at right angles to the deep penetrating branch that occurs with it, the doublestem artery, and this anatomical structure makes the vessel prone to rupture and bleeding when the blood pressure rises abruptly due to force and excitement.