Radiation brain injury is a common complication arising from the treatment of intracranial tumors, cerebrovascular malformations, and malignant tumors of the head and neck. With the widespread use of radiological techniques such as linear gas pedal, X-knife, γ-knife, photon knife, and inter-tissue brachytherapy in clinical work, the incidence of radiation brain injury has gradually increased. With the development of magnetic resonance spectroscopy (MRS), single photon emission computed tomography (SPECT) and positron emission tomography (PET), the diagnosis and treatment of radiation brain injury has made a great leap forward, and the adjustment of radiation therapy intensity has also been emphasized by radiation therapy specialists, thus enhancing the understanding of radiation brain injury. Now only the occurrence mechanism, imaging changes and treatment progress are reviewed as follows. 1, the mechanism of occurrence The mechanism of occurrence of radiation brain injury is not very clear, and may be related to the following factors. （Kurita et al. found that apoptosis of leukocytes in adult rat brain peaked 8h after radiation, mainly apoptosis of oligodendrocytes, resulting in impaired renewal and replacement of oligodendrocytes, thus causing demyelination. (2) Secondary ischemia and necrosis of brain tissue caused by vascular injury The pathology of radiation brain injury includes reactive intimal hyperplasia, thickening, wall thickening and lumen narrowing, mostly involving small and medium-sized arteries, but also involving large vessels such as the internal carotid artery. We found that the capillary network in the irradiated area was thickened and the basement membrane vacuoles were formed. It is believed that vascular changes are the basis of radiation damage. Progressive vascular lesions can explain the long latency period of radiation brain injury and the secondary damage to brain tissue outside the irradiated area. (3) Autoimmune reaction In some cases, neural tissue has a high sensitivity to radiation, and an autoimmune reaction may occur, which eventually leads to demyelination. (4) Free radical damage Radiation alters the activity of some enzymes in the tissues, leaving them in a dysfunctional state. The involvement of free radical damage and immune response causes slow, persistent and progressive pathological changes, which can also explain the long latency period of radiation brain injury. Most scholars believe that these mechanisms are not independent of each other, but are multifactorial. According to the time of radiation therapy reaction, radiation brain injury is divided into acute phase, early delayed reaction and late delayed reaction. The acute phase (hours-3 weeks) is rare clinically, mainly due to the damage of blood-brain barrier and increased permeability, resulting in cerebral edema, increased intracranial pressure and transient neurological dysfunction, etc., which can generally heal spontaneously. The histological changes in this stage are mainly due to the damage of vascular endothelium, which is the most sensitive to radiation and is most easily damaged. In addition, acute radiation brain injury is closely related to single dose, single dose >3Gy and excessive volume of exposure can significantly increase the incidence of acute radiation brain injury. The early delayed reaction (3 weeks-3 months) is mainly demyelination of oligodendrocytes with axonal edema. The clinical manifestations are usually drowsiness and mental disturbance, which can be recovered with treatment. In the late stage of late reaction (3 months to several years), there are two types of radionecrosis: limited radionecrosis and diffuse radionecrosis, mainly glassy and fibrinoid necrosis of small blood vessels, accompanied by luminal narrowing, intimal hyperplasia, perivascular edema, thrombosis and patchy hemorrhage, with varying degrees of calcification in the white matter. The most characteristic histological changes of advanced radionecrosis are eosinophilic cells and fibrin exudation, which spread along the gray-white matter junction. The clinical manifestations are limited neurological dysfunction and progressive aggravation, motor and sensory impairment of one limb, aphasia, epilepsy, mental retardation and psychiatric abnormalities. 3, imaging diagnosis (1) MRI and CT radioactive brain injury in general MRI and CT performance is not specific, CT scan shows the lesion is hypointense, the edema around the lesion is obvious, MRI scan T1WI most of the low signal, in T2WI parenchymal part of the low signal area, and the central necrotic area is high signal. Due to the abnormal permeability of the blood-brain barrier, the area of radiation necrosis can be enhanced on CT and MRI, which makes it difficult to distinguish from tumor recurrence. (2) MRS is a non-invasive technique to detect the content of compounds in human body, which is different from the traditional imaging technique of MR, because the frequency distribution curve of chemical shifts of compounds or monomers is used to express the examination results, instead of showing the lesion by grayscale contrast of images. It is valuable for differentiating radiation brain injury from tumor recurrence. Currently, proton magnetic resonance spectroscopy (1HMRS) is commonly used in clinical and research brain tests. The metabolites measured are aspartate (NAA), creatine (Cr), phosphocreatine (PCr), choline (Cho), inositol (MI), lactate (Lac), and lipids (Lip). In radionecrosis, NAA/Cr and NAA/Cho were both decreased, while Cho/Cr was significantly increased. A progressive decrease in NAA tended to indicate more severe brain damage. In the case of in situ tumor recurrence, Cho was mainly increased, while peaks of choline and lactate in necrotic tissue were absent. Thus, choline is the most important metabolite to distinguish tumor recurrence from radiation damage, especially for the determination of choline values before and after radiotherapy. However, in patients with glioma after radiotherapy, it is prudent to use 1HMRS to evaluate brain damage and tumor recurrence, especially in glioma with high malignancy. (3) Magnetic resonance perfusion imaging (MRP) Magnetic resonance perfusion imaging is an MR dynamic imaging performed after intravenous injection of high concentration of Gd-DTPA to evaluate the state and function of capillary beds. It is mainly used clinically to evaluate the malignancy of tumors and to identify whether MRI after radiation therapy shows a response to radiation therapy, scar suppression, or tumor recurrence. Measurement of local cerebral blood flow velocity (rCBV) provides pathological vascular information to accurately identify tumor recurrence and radiation necrosis. rCBV information lacking neovascularization tends to be more closely associated with radiation necrosis and vice versa, suggesting tumor recurrence. sugahara et al. applied MRP to measure the relative blood flow volume ratio of brain enhancement area speciation after radiation therapy for brain tumors and found that including radiation brain injury non When the rCBV ratio was between 0.6 and 2.6, MRP was unable to identify the tumor and further 201 T-SPECT must be performed. (4) SPECT SPECT and PET are brain imaging techniques using radiopharmaceutical reagents, which are classified according to blood-brain barrier altering permeant, normal brain cell diffusing agent, metabolic receptor binding agent and antigen-antibody binding agent. ). Radiation necrosis is generally not isotopically concentrated, with LPN values (LesionPNormal) <2.5, while in the tumor area there is usually isotopic concentration, with LPN >2.5, the mechanism of which is unclear. 22 patients were examined by Lamy-Lhullier et al. using 99mTc as a tracer to identify radiation necrosis or tumor recurrence and to compare the results with subsequent biopsies or clinical follow-up. The sensitivity and specificity of PET PET were 73%, 85%, 91% positive predictive value, and 60% negative predictive value, which were found to be able to identify tumor recurrence, but negative results were not significant. (5) PET PET can understand the integrity of blood-brain barrier and cerebral circulation perfusion and the metabolism of oxygen, glucose and amino acid. In clinical practice, 18F-fluorodeoxyglucose (18F-FDG) is often used to reflect the glycolytic rate of cells, and methionine MET is used to determine the metabolism of amino acids, etc. The metabolic rate of radiation necrosis is lower than that of normal brain tissue, and the uptake of FDG or MET is usually reduced, while the uptake in the tumor area is significantly increased. The sensitivity and specificity of 18F-FDG were 75% and 81% for all tumors, and 65% and 80% for brain metastases. 86% sensitivity and 80% specificity were obtained for 18F-FDG combined with MR. It was concluded that 18F-FDG combined with MRI could effectively identify necrotic and recurrent brain metastases. However, MRI is more sensitive than CT in the visualization of lesions, especially in the observation of the extent of edema, and is preferred when imaging changes of radiation brain injury are present. MRP and MRS have diagnostic significance for detecting changes in the acute and early late-onset phases of radiation brain injury. The initial treatment is based on cortisol, the mechanism of which is anti-inflammatory, anti-edema, reducing cytokine release and inhibiting immune response. It helps to stabilize the integrity of capillaries, but cannot stop the clinical process of radiation brain injury. In the early stage, when cerebral edema is the main manifestation, hormonal therapy is effective, but the duration of treatment is usually long, more than 3 months, so it increases the risk of some complications, such as infection, proximal muscle weakness, osteoporosis, etc. Kondziolka et al. studied the effect of 21-amino acid steroid U-74389G on radiation brain injury and found that high doses (15 mg/kg) of U-4389G had The protective effect was found in the high dose (15 mg/kg) of U-4389G and was most pronounced in the 100 Gy dose group. GM1 is a cell membrane lipid stabilizer, which can effectively block the direct damage of ionizing radiation and secondary free radical damage after radiotherapy, promote neural repair, and thus improve clinical symptoms. The therapeutic effect of GM1 on radioactive brain injury may be achieved by activating the activity of Na+-K+-ATP enzyme, reducing the outflow of K+ and Ca2+ from the membrane, preventing membrane lipid hydrolysis, and blocking the free radical cycle of cell membrane lipid peroxidation. (2) Hyperbaric oxygen can increase the partial pressure of oxygen in tissues, stimulate the production of endothelial growth factor, and activate the cellular and vascular repair mechanism. 74 cases of hyperbaric oxygen treatment for radiation brain injury were analyzed by Feldmeier et al. Therefore, it is believed that hyperbaric oxygen can be used as a routine treatment for radiation brain injury, and it should be performed simultaneously with drug therapy. (3) Surgery Patients with radiation brain necrosis who have progressive neurological dysfunction, increased intracranial pressure, long-term reliance on hormone therapy, and imaging suggestive of extensive cerebral edema and occupational effects may be treated surgically to remove necrotic tissue. When it is difficult to distinguish between tumor recurrence and radiation brain necrosis, and the occupying effect of the lesion is more obvious, the lesion should also be actively removed surgically.