As the tumor gradually increases, it forms intracranial occupying lesions and is often accompanied by peripheral cerebral edema, which will produce increased intracranial pressure when it exceeds the compensatory limit. When the tumor obstructs the cerebrospinal fluid circulation or compresses the vein, which leads to the obstruction of venous return, the intracranial pressure increases even more. If hemorrhage, necrosis and cyst formation occur in the tumor, the process can be accelerated. When the increase of intracranial pressure reaches the critical point, the intracranial volume continues to have a small increase and the intracranial pressure will increase rapidly. If intracranial pressure monitoring is performed, when the pressure reaches 6.67-13.3 kpa Hg, plateau wave appears, and plateau wave appears repeatedly and lasts for a long time, which is the clinical sign. When intracranial pressure equals to arterial pressure, cerebrovascular paralysis, cerebral blood flow stops, blood pressure drops, and the patient will die soon. When the tumor increases, the local intracranial pressure will be the highest and the pressure gradient between the intracranial compartments will cause brain displacement, which will lead to brain herniation if it is gradually aggravated. Tumors in the supratentorial cerebral hemispheres can produce subfalx herniation, and the cingulate gyrus can move past the midline, resulting in wedge-shaped necrosis. The pericallosal artery may also be displaced by pressure, and cerebral infarction may occur in the supply area in severe cases. More importantly, the medial temporal lobe gyrus herniates through the cerebellar tract to the posterior cranial fossa. The ipsilateral arteriolar nerve is paralyzed by compression, the pupil is dilated, and the light response is lost. Compression of the cerebral peduncle of the midbrain produces contralateral hemiparesis. Sometimes the contralateral cerebral peduncle is compressed on the edge of the cerebellar curtain or the tip of the bone, producing ipsilateral hemiparesis. The posterior choroidal artery and posterior cerebral artery may also be compressed causing ischemic necrosis. Finally, compression of the brainstem may produce downward axial displacement, leading to infarct hemorrhage in the midbrain and upper pontine brain. The patient becomes comatose, blood pressure rises, pulse is slow, breathing is deep and irregular, and decerebrate brain tonicity may occur. Eventually death occurs with respiratory arrest, decreased blood pressure, and cardiac arrest. Inferior posterior cranial fossa tumor may produce herniation of the greater occipital foramen and downward displacement of cerebellar tonsils herniating out of the greater occipital foramen. In severe cases, the medulla oblongata ventrally compresses the anterior border of the foramen magnum. Supratentorial tumors may also herniate the foramen magnum. The patient becomes unconscious, blood pressure rises, pulse is slow and strong, and breathing is deep and unplanned. Subsequently, respiration stops, blood pressure drops, pulse is rapid and weak, and death eventually occurs.