Radiation encephalopathy is a disease of the central nervous system caused by the exposure of brain tissue to radiation and the combination of multiple factors that lead to degeneration and necrosis of neurons. Radiation encephalopathy can occur during radiation treatment for a variety of disorders such as brain tumors, extracranial (nasopharyngeal carcinoma) or leukemic encephalopathy. Radiation encephalopathy seriously affects the survival time and quality of life of patients and is the most serious complication after radiotherapy treatment. Why do some people develop radiation encephalopathy while others do not when they also receive radiation therapy? We have proved through experiments that the occurrence of radiation brain injury is closely related to the radiation source, total radiation dose, fractional dose, length of treatment, irradiation area, age and so on. Among many factors, the total radiation dose is more significant than other factors; in the case of the same total dose, the single high-dose irradiation is more dangerous than multiple high-dose irradiation; the radiation sensitivity of brain tissue of minors is also higher than that of adults. The total dose splitting and the total treatment time are closely related. In addition, the occurrence of radiation encephalopathy is also related to the physical condition, the degree of vascular sclerosis, the number of irradiation, the immune status of the body, and whether or not chemotherapy is applied in combination. How does radiation encephalopathy occur? There are four theories about the pathogenesis of radiation encephalopathy: 1. Neuronal damage theory It is generally believed that mature neuronal cells have high tolerance to ionizing radiation, while neurons in the developmental period (embryonic and neonatal period) have higher sensitivity to ionizing radiation. Related experiments have shown that neuronal cells can show changes on day 3 after radiation, mainly chromatin sparing and edema of cells, and obvious apoptotic changes can be seen on day 7. Some studies have also shown that neuronal cells are more sensitive to radiation than glial cells in the early stage of radiation brain injury. 2, glial cell damage theory This theory believes that the typical pathological changes of radiation encephalopathy are mainly demyelination. Myelin is mainly composed of oligodendrocytes, and obviously, the death of oligodendrocytes is the main cause of demyelination. O-2A cells are the precursor cells of oligodendrocytes, and 5Gy irradiation can reduce the proliferation capacity of O-2A progenitor cells, and the dead oligodendrocytes are not renewed in time, which causes demyelination. The loss of O-2A cells is also time- and dose-dependent. In addition, astrocytes and microglia have an important role in maintaining the normal structural and functional state of neurons. Both types of cells exhibit a proliferative response 1 to 2 weeks after irradiation. Subventricular zone cells are the main source of neurons, astrocytes and oligodendrocytes from embryo to adult. Animal studies have shown that the hippocampus and subventricular zone are the most sensitive areas of the central nervous system to radiation. It can be seen that the destruction of cells in the subventricular zone will affect the degree of radioactive brain damage and recovery. This theory can well explain the phenomenon that radiation necrosis occurs mostly in the white matter, but it cannot explain the damage outside the irradiation site, even in the distant septum, and the occurrence of late onset necrosis. Pena LA et al. irradiated the whole brain of mice with a single high dose (5-100Gy), and the volume of vascular endothelial cells increased, nuclear consolidation and fragmentation, and the number of endothelial cells decreased in the early stage after irradiation, and the change was time- and dose-dependent; perivascular inflammatory cells adhered and infiltrated. In the early stage after irradiation, the endothelial cells increased in size, nuclear consolidation and fragmentation, and the number of endothelial cells decreased. In the late post-irradiation period, vascular wall thickening, lumen dilation, capillary atrophy, scar formation and fibrosis affect the local blood flow and energy supply to the brain, and accelerate the liquefaction and necrosis of brain tissue. Vascular damage is the main pathological basis of late radiation brain injury. According to the basic view of this theory, the gray matter, which is the most sensitive to ischemia, should be the most susceptible to necrosis, however, this is not the case, and necrosis is common in the white matter, so it cannot be said that vascular injury is the only pathological mechanism of brain white matter radiation necrosis. 4, autoimmune reaction Autoimmune reaction, oligodendrocytes and their enzyme system produce autoantigens after illumination. The autoimmune reaction is induced, leading to changes such as demyelination and brain edema. The complexity of the composition of the central nervous system determines the complexity of radioencephalopathy lesions, and no single factor can fully explain the pathogenesis. The pathogenesis of radiation brain injury has been a hot spot of clinical research, and some scholars have tried to reveal the mechanism of radiation brain injury at the molecular and genetic levels. Some results show that apoptosis, free radical damage, calcium inward flow, cytokines, mutations in some specific genes, and changes in related enzyme activities are involved in the occurrence and progression of radiation encephalopathy.