Hypertensive cerebral hemorrhage (HCH) is one of the most common forms of cerebrovascular disease with a high mortality and disability rate, and more than 3/4 of survivors have varying degrees of disability. The age of onset of hypertensive cerebral hemorrhage is usually 50-60 years old, but it can also occur in patients with hypertension in their 30s and 40s. Hypertensive cerebral hemorrhage often occurs at the age of 45-65 years, and is slightly more common in men than in women. It often occurs during emotional excitement, overexcitement, defecation, breath-holding or mental stress. Brain hemorrhage is often unpredictable, occurs suddenly, and has a rapid onset, often developing to a peak within minutes to hours. It is less common for the disease to progress to a severe level over a longer period of time. The onset of hemorrhage is usually characterized by severe head pain, followed by frequent vomiting, systolic blood pressure of 180 mmHg or more, occasional convulsions, etc. In severe cases, the mind often turns into coma within minutes or tens of minutes, accompanied by fecal and urinary incontinence. If the pulse rate is rapid and the blood pressure drops, it is a sign of endangerment. This disease, which mainly affects the elderly, is a serious threat to people’s health. Therefore, it must be taken seriously and effective measures for its prevention and treatment must be continuously researched. Hypertensive cerebral hemorrhage is 80% above the curtain and 20% below. Hemorrhage in the cerebral hemispheres is most common in the basal nucleus and optic thalamus, followed by the brainstem and cerebellum. The rate of hemorrhage, the amount of hemorrhage, and the site of hemorrhage vary, leading to different clinical manifestations in patients. 1. Hemorrhage in the nucleus accumbens and basal ganglia Hemorrhage in the nucleus accumbens and basal ganglia is the most common site of hypertensive cerebral hemorrhage, mostly affecting the internal capsule, and the patient often has the head and eyes turned to the side of the hemorrhagic lesion, showing “focal gaze” and “triple hemianopia”, i.e. hemiparesis, hemianesthesia and hemianopsia. and hemianopia. In the early stage, the muscle tone and tendon reflexes of the paralyzed limb decreased or disappeared, and then gradually became higher, the upper limb was flexed and retracted, the lower limb was stretched and straightened, the tendon reflexes became hyperactive, ankle clonus could occur, and the pathological reflexes were positive. The hemorrhagic focal point contralateral to the hemorrhagic focal point is hyperalgesia, and the response to needling the limb and face is unresponsive or slower than that of the other side. If the patient is clear and cooperates with the examination, ipsilateral hemianopia contralateral to the lesion may also be found. If the hematoma breaks into the lateral ventricle, or even fills the whole lateral ventricle, it is called lateral ventricular cast, and its prognosis is poor. 2. Cerebral bridge hemorrhage Cerebral bridge hemorrhage often starts suddenly and enters deep coma within a few minutes, and the condition is critical. Cerebral bridge hemorrhage often starts from one side of the cerebral bridge, and then spreads to both sides quickly, resulting in bilateral limb paralysis. Most of them are flaccid, a few are spastic or decorticate tonic, and bilateral pathological reflexes are positive. The characteristic sign is extreme narrowing of the pupils on both sides in a “pinpoint” fashion. Some patients may develop central hyperthermia, irregular breathing and respiratory distress, and often die within 1-2 days. 3, cerebellar hemorrhage The mild type of patients are clear-headed at the beginning, often complaining of severe headache and vertigo in the posterior occipital region, frequent vomiting, slurred pronunciation, and nystagmus. The limbs are often not paralyzed, but ataxia occurs in the limb on the side of the lesion. When the hematoma gradually enlarges and breaks into the fourth ventricle, it may cause acute hydrocephalus. In severe cases, herniation of the foramen magnum occurs, and the patient suddenly falls into coma, has irregular breathing or even stops, and eventually dies due to respiratory and circulatory failure. In addition, primary or secondary damage occurs in the brainstem, especially in the lower thalamus. It can occur including cerebro-cardiac syndrome, acute gastrointestinal hemorrhage, central respiratory form abnormalities, central pulmonary edema and central eruption. The presence of these syndromes often affects the prognosis and can lead to death in severe cases.