Bleeding in the brain parenchyma is called cerebral hemorrhage (ICH). It is bleeding from lesions in the arteries, veins and capillaries of the brain. Arterial hemorrhage is the most common. Blood accumulates in the brain parenchyma to form an intracerebral hematoma. The most common cause of spontaneous cerebral hemorrhage is hypertension. Patients with hypertension have about 1/3 chance of developing cerebral hemorrhage, and 93.91% of patients with cerebral hemorrhage have a history of hypertension. The main clinicopathological course of intracerebral hemorrhage is related to the site of bleeding. In a small amount of bleeding, blood only penetrates between the nerve fibers and causes less damage to the brain tissue; in a larger amount of cerebral hemorrhage, blood accumulates in the brain to form a hematoma, which can form cerebral edema and intracranial hypertension within a few hours, causing the adjacent tissues to be displaced by the pressure to the formation of brain herniation, while causing the brain tissue to be hypoxic. Intracerebral hematoma and cerebral edema can compress the ventricles inward and displace them, and compress the thalamus and hypothalamus downward, causing severe autonomic dysfunction symptoms. In the case of supratentorial hematoma, the risk of midbrain compression is high; in the case of cerebellar hematoma, the medulla oblongata is easily compressed by the lower herniated cerebellar tonsils. Intracerebral hematoma may break into the ventricle or subarachnoid space, forming secondary ventricular hemorrhage and secondary subarachnoid hemorrhage. Clinical manifestations of cerebral hemorrhage: Hypertensive cerebral hemorrhage is most frequent in hypertensive patients around 50 years of age. Because of the close relationship with hypertension, it can occur in young hypertensive patients, even in their 30s. Although cerebral hemorrhage can sometimes occur at rest or during sleep, it usually develops immediately during the day when physical or mental activity is intense, such as emotional excitement or excessive exertion. Apart from dizziness, headache, poor work efficiency, rhinorrhea and other symptoms of hypertension, the general physical condition is usually not special. There is often no premonition before the occurrence of cerebral hemorrhage. Very few patients complain of cerebral symptoms such as transient or transient blurring of consciousness, difficulty in movement of arms and legs or slurred speech several hours or days before bleeding. Hypertensive cerebral hemorrhage often occurs suddenly, with a rapid onset, and often progresses to a peak within minutes to hours. The clinical manifestations depend on various factors such as the site of hemorrhage, the extent of hemorrhage, the body’s response, and the systemic condition. (A) Internal capsule hemorrhage: The basal ganglia of the brain is the most common site of hemorrhage, which is called internal capsule hemorrhage because of the damage to the internal capsule. In addition to the general symptoms of cerebral hemorrhage, patients with internal capsule hemorrhage often have the head and eyes turned to the side of the hemorrhagic lesion, showing “staring at the lesion” and the symptoms of “three deviations”, namely hemiparesis, hemianesthesia and hemianopsia. The hemiplegic limb on the opposite side of the hemorrhage becomes paralyzed, the nasolabial groove on the paralyzed side is shallow, and the cheeks on the paralyzed side bulge higher during exhalation. The paralyzed limb gradually turns from flaccid to spastic, the upper limb is flexed inward, the lower limb is tonic, the tendon reflex turns hyperactive, ankle clonus may appear, and the pathological reflex is positive, showing typical upper motor neurogenic hemiparesis. 2, hemianesthesia hemorrhagic foci contralateral hemianesthesia, no response when needling the limb or face or the response is dull compared with the other side. 3, hemianopia can be found when the patient’s state of consciousness can cooperate with the examination, which is mainly due to the involvement of the visual radiation through the internal capsule. In addition, patients with primary cerebral hemisphere lesions often associated with aphasia brain hemorrhage can also develop parietal syndromes, such as somatosomatic disorders (hemiplegic agnosia, phantom multiple limbs, illusory limb displacement, etc.), loss of structure, geographic disorientation, etc. Intelligent activities such as memory, analytical comprehension, and calculation are often significantly diminished after cerebral hemorrhage. (b) Pontocerebral hemorrhage: It often starts suddenly with severe headache, dizziness, blurred vision, falling to the ground, vomiting, diplopia, nausea, difficulty in swallowing, and numbness on one side of the face. Consciousness may be partially preserved at the beginning of the illness, but often enters a deep coma within minutes. Hemorrhage often starts on one side of the pontine brain and manifests as crossed paralysis, i.e., lateral paralysis of the hemorrhage side and flaccid paralysis of the contralateral upper and lower extremities. The head and eyes are turned to the non-hemorrhagic side in a “gaze paresis” pattern. Pontocerebral hemorrhage often spreads rapidly to both sides, resulting in facial and limb paralysis on both sides, with most of the limb paralysis being flaccid. Most of the limb paresis is flaccid, but a few are spastic or decerebrate. Bilateral pathological reflexes are positive. The head and eyes return to a central position, and the pupils on both sides are extremely narrowed. This “pinpoint” pupil is seen in 1/3 of patients with pontocerebral hemorrhage and is a characteristic symptom due to damage to sympathetic nerve fibers in the pontocerebrum. Pontocerebral hemorrhage often blocks the normal regulation of body temperature by the lower thalamus, resulting in a severe rise in body temperature and a persistent hyperthermia. Irregular breathing often occurs due to the influence of the brainstem respiratory center, and respiratory distress may appear at an early stage. After pontocerebral hemorrhage, the condition is critical if the pupils on both sides are dilated, the reflex to light disappears, the breathing is irregular, the pulse and blood pressure are dysregulated, and the body temperature keeps rising or suddenly falls. (iii) Cerebellar hemorrhage: Most cerebellar hemorrhages occur in one cerebellar hemisphere, which can lead to acute intracranial pressure increase, brainstem compression, and even occipital foramen herniation. The onset of hemorrhage is rapid, and a few of them are so dangerous that they may immediately fall into a deep coma and stop breathing within a short period of time. Most patients are clearly conscious at the onset of the disease, often complaining of severe headache and vertigo on one side of the posterior occipital region, frequent vomiting, and slurred pronunciation. The pupils are often narrowed, and both eyes gaze in the same direction to the opposite side of the lesion. Ataxia of the limb movements on the side of the lesion, but paralysis is not obvious. There may be symptoms of cranial nerve palsy and cervical tonicity. The disease gradually worsens, the consciousness becomes blurred or comatose, and the breathing is irregular. (iv) Ventricular hemorrhage: Most of the ventricular hemorrhages are due to hemorrhage in the basal ganglia of the brain and then break into the lateral ventricles, so that the blood fills the entire ventricle and the subarachnoid system. Cerebellar hemorrhage and pontocerebellar hemorrhage may also break into the fourth ventricle. This is an extremely serious condition. Consciousness often lapses into a deep coma within 1-2 hours, with tetanic seizures or tetraplegia. Bilateral pathological reflexes are positive. Quadriplegia is often flaccid, and all tendon reflexes are not elicited may appear paroxysmatically as tonic spasms or decerebrate tonic states. Breathing is deep with snoring and later turns shallow, rapid and irregular.