The duration of the disease is often influenced by various factors, such as age, lesion location, nature of the lesion, growth rate, the degree of cerebral edema and the patient’s general condition. In the process of intracranial pressure increase, it is also often affected by the presence of certain vicious circle factors, which can lead to the prolongation of the course of intracranial pressure increase or rapid deterioration of the disease, to be diagnosed when serious symptoms and signs appear, resulting in treatment difficulties or lost treatment opportunities and poor prognosis. 1.Age The age of onset of disease, intellectual development and language expression may affect the course of intracranial hypertension. For example, when the fusion of cranial suture is not completely solid in children and adolescents, the increased intracranial pressure can separate the cranial suture; in infants and children, the cranial suture and anterior chimney are not closed, and the increased intracranial pressure can increase the volume of cranial cavity and make the compensatory space of cranial volume expand. When there are intracranial occupational lesions or other causes of cranial content volume increase, the symptoms and signs of intracranial pressure increase may appear later due to the increase of cranial cavity volume; or there are early mild symptoms and signs, which are ignored due to immature intelligence (including language), poor expression ability and lack of medical knowledge of relatives, thus delaying the course of intracranial pressure increase. Children with congenital hydrocephalus, for example, are not seen until the head is quite large or when more severe neuropsychiatric symptoms and signs appear. Patients with substantial brain atrophy (common in the elderly), because of brain atrophy, brain volume reduction, so that the volume of the cranial cavity compensatory space relatively expanded, such as intracranial occupying lesions or other reasons caused by the increase in the volume of cranial contents, in a considerable period of time may not appear obvious signs and symptoms of increased intracranial pressure, so the course of the disease can be relatively extended. For example, in acute subdural hematoma, when the midline is displaced by 10mm, the intracranial pressure can be increased up to 6.67kPa (50mmHg); while in chronic subdural hematoma or benign tumor, when the midline is displaced by 20mm, the intracranial pressure may still be increased insignificantly. This is mainly due to the different speed of intracranial pressure increase and the different role played by intracranial space compensatory mechanism, especially for benign tumor, which grows slowly and the intracranial pressure increase appears later, while the brain tissue can slowly shrink due to tumor compression, which prolongs the course of the disease. If malignant tumor or metastatic tumor grows faster, the symptoms of intracranial pressure increase also appear faster and the disease course is relatively short. In some other destructive or infiltrative lesions, although the lesion itself is expansive, the net increase in the volume of cranial cavity contents is not significant because it destroys the surrounding brain tissues, so that the symptoms of increased intracranial pressure do not appear or are delayed despite the rapid development of clinical symptoms. Lesions located in the ventricular system, midline area or posterior cranial fossa tend to block the cerebrospinal fluid circulation pathway and affect the absorption of cerebrospinal fluid, therefore, although the lesion volume itself may not be large, the increase in intracranial pressure often occurs early or aggravates the existing increase in intracranial pressure due to hydrocephalus. The lesions located near the large intracranial venous sinuses can also cause the symptoms of increased intracranial pressure to appear early because they can compress the venous sinuses at an early stage and obstruct the return of intracranial venous blood or the absorption of cerebrospinal fluid. 4.The extent of intracranial lesions with cerebral edema Inflammatory intracranial lesions, such as brain abscess, brain parasitosis, brain tuberculoma, brain granuloma, diffuse meningitis and encephalitis, can be accompanied by obvious cerebral edema; malignant brain tumors, especially brain metastatic carcinoma, are commonly not large in size but accompanied by more serious cerebral edema, which can lead to the early appearance of increased intracranial pressure. 5. Systemic conditions Severe systemic diseases, such as uremia, hepatic coma, various kinds of toxemia, pulmonary infection, acid-base balance imbalance, etc., can cause secondary cerebral edema and contribute to the increase of intracranial pressure. If respiratory insufficiency or respiratory depression causes cerebral tissue hypoxia and increased carbonic acid, cerebral vasodilation and cerebral edema can be secondary, leading to increased intracranial pressure, which in turn reduces cerebral blood flow, exacerbates respiratory depression and cerebral hypoxia, and further aggravates increased intracranial pressure. Severe increase in intracranial pressure can cause brain herniation, and brain tumor can aggravate cerebrospinal fluid and cerebral blood circulation disorders, resulting in higher intracranial pressure, which in turn contributes to more severe brain herniation. Systemic hyperthermia can also aggravate the degree of increased intracranial pressure.