Cerebral hemorrhage is a non-traumatic hemorrhage caused by rupture of blood vessels in the brain parenchyma, accounting for 20%-30% of all strokes. The cause of occurrence is mainly related to cerebral vascular lesions, i.e., closely related to hyperlipidemia, diabetes, hypertension, aging of blood vessels, smoking, etc. Patients with cerebral hemorrhage often have a sudden onset due to emotional stress and strenuous exertion, and the early mortality rate is high, and most of the survivors are left with sequelae such as motor impairment, cognitive impairment, and speech and swallowing disorders of varying degrees. The common cause is hypertension combined with small arteriosclerosis, other causes include cerebrovascular malformation, aneurysm, hematologic disease, vasculitis, aneurysmal stroke, etc. Overexertion, climate change, alcohol consumption, emotional stress, and overexertion are the triggering factors. Hypertensive cerebral hemorrhage is one of the most serious complications of hypertensive disease, which often occurs at the age of 50-70, slightly more in men, and more likely to occur in winter and spring. Hypertensive disease often leads to pathological changes in the small arteries at the base of the brain, highlighted by glassy or fibrous degeneration and focal hemorrhage, ischemia and necrosis in the walls of these small arteries, weakening the strength of the vessel walls, appearing as a limited dilatation and forming tiny aneurysms. The rupture and bleeding of an already diseased cerebral vessel is caused by a violent increase in blood pressure due to emotional excitement, excessive mental and physical labor, or other factors. The rupture of the pulsatile artery is the most common, followed by the thalamic penetrating artery, thalamic geniculate artery, and posterior internal choroid plexus artery. Increased blood pressure is the underlying cause and usually develops during activity and emotional stress. The vast majority of scholars believe that long-term hypertension can cause vitreous degeneration of cerebral arteries, which begins with swelling of the subintimal matrix, subintimal lipid deposits, formation of structureless material between the intima and the internal elastic layer, reduced elasticity, and increased brittleness. The loss of vessel wall tension and fibrinoid necrosis produce local arterial fusiform or spherical projections under blood pressure shock, i.e., cornual aneurysms, and blood may also invade the vessel wall and form a sandwich aneurysm. When the blood pressure rises suddenly, the aneurysm ruptures and causes bleeding. In addition, hypertension can also cause spasm of small cerebral arteries, resulting in ischemia, hypoxia, and necrosis of distal brain tissue, producing hemorrhage. In addition, weak walls of the intracerebral arteries, with few middle layer myocytes and outer membrane connective tissue and no outer elastic layer, may lead to more cerebral hemorrhage in hypertension than other internal bleeding.