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 been emphasized by radiation therapy specialists, thus enhancing the understanding of radiation brain injury. The following is a review of the mechanism of occurrence, imaging changes and treatment progress. 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. (1) direct damage to brain tissue by radiation: rapidly dividing cells are particularly sensitive to radiation, and Kurita et al. found that apoptosis of white matter cells peaked 8 h after radiation in adult rats, with apoptosis of oligodendrocytes being the main cause, resulting in impaired renewal and replacement of oligodendrocytes, thus causing demyelination. (2) Vascular injury causes secondary brain tissue ischemia and necrosis: The pathology of radioactive 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. They found that the capillary network in the irradiated area was thickened, the basement membrane was vacuolated, and the capillary density was lower than that in the unirradiated area. It is believed that vascular changes are the basis of radiation damage. Progressive vascular lesions can explain the long latency period of radioactive brain injury and the secondary damage of brain tissue outside the irradiated area. (3) Autoimmune reaction: In some cases, neural tissue has a high sensitivity to radiation and can develop an autoimmune reaction, which eventually leads to demyelination. (4) Free radical damage: Radiation alters the activity of some enzymes in the tissue, leaving it 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 the above mechanisms are not independent of each other, but are multifactorial. 2, pathological histological basis and clinical According to the time of appearance of radiotherapy reaction, radiation brain injury is divided into acute phase, early delayed reaction and late delayed reaction. The acute phase (several 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. Histological changes in this stage are mainly damage to the vascular endothelium, which is due to the fact that vascular endothelial cells are more sensitive to radiation and are most easily damaged. In addition, acute radiation brain injury is closely related to single dose, and single dose >3Gy and excessive volume of irradiation can significantly increase the incidence of acute radiation brain injury. Early delayed reaction (3 weeks-3 months), mainly demyelinating lesions of oligodendrocytes with axonal edema. The clinical manifestations are mostly drowsiness and mental disturbance, which can be recovered with treatment. Late stage late reaction (3 months – several years), divided into two categories: limited radionecrosis and diffuse radionecrosis, mainly glassy and fibrinoid necrosis of small 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 fibrinous exudates that 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 may occur. 3, imaging diagnosis (1) MRI and CT: the performance of projectile brain injury on general MRI and CT is mostly non-specific, CT scan shows the lesion is hypointense, the edema around the lesion is obvious, MRI scan on T1WI is mostly low signal, in T2WI parenchymal part has low signal area, while the central necrotic area shows high signal. Due to the abnormal permeability of the blood-brain barrier, the area of radiation necrosis can also be enhanced on CT and MRI, thus making it difficult to distinguish from tumor recurrence. (2) MRS: MRS examination is a non-invasive technique to detect the content of compounds in human body, which is different from the traditional imaging technique of MR, it represents the examination results by the frequency distribution curve of chemical shifts of compounds or monomers, instead of showing the lesions by the grayscale contrast of images. It is valuable to distinguish radiological brain injury from tumor recurrence. Currently, proton magnetic resonance spectroscopy (1HMRS) is commonly used in clinical and scientific research for brain detection. Its metabolites measured are aspartate (NAA), creatine (Cr), phosphocreatine (PCr), choline (Cho), inositol (MI), lactate (Lac), lipids (Lip), etc. In radiation necrosis, both NAA/Cr and NAA/Cho are decreased, while Cho/Cr is significantly increased. A progressive decrease in NAA is often indicative of more severe brain damage. In situ tumor recurrence is mainly an increase in Cho, whereas peaks in choline and lactate in necrotic tissue are absent. Thus, choline is the most important metabolite to identify tumor recurrence and radiation damage, especially for the determination of choline values before and after radiotherapy. However, it is prudent to use 1HMRS only to evaluate brain injury and tumor recurrence in patients with glioma after radiotherapy, especially to evaluate 1HMRS in glioma with high malignancy, which sometimes leads to conclusions contradictory to the above conclusions. (3) Magnetic resonance perfusion imaging (MRP): MRP is a dynamic MR 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 for the evaluation of tumor malignancy and to identify whether the MRI seen after radiotherapy is a response to radiotherapy, scar suppression, or tumor recurrence. Measurement of local cerebral blood flow maps (rCBV) can provide pathologic 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 relative blood flow volume ratios in brain enhancement areas speciated after radiotherapy 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. isotope markers generally used for SPECT are 99mTc-methoxyisobutylisocyanide (99mTc-MIBI) and 201 thallium ( 201TI). Radiation necrosis is generally not isotopically concentrated, with an LPN value (LesionPNormal) <2.5, while in the tumor area there is usually isotopic concentration, with an LPN >2.5, the mechanism of which is unclear. It was found that the sensitivity of detecting tumor recurrence was 73%, the specificity was 85%, the positive predictive value was 91%, and the negative predictive value was 60%, and the positive result could basically identify tumor recurrence, but the negative result was 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 applied to reflect the rate of cellular glycolysis, and methionine MET is applied to determine the metabolism of amino acids, etc. The metabolic rate of radiation necrosis is lower than that of normal brain tissue, and usually the uptake of FDG or MET is reduced, while the uptake in the tumor area is significantly increased. Chao et al. used 18F-FDG to study 47 cases of tumors after receiving stereotactic radiation therapy. The sensitivity and specificity of 18F-FDG was 75% and 81% for all tumors, and 65% and 80% for brain metastases. 18F-FDG combined with MR showed a sensitivity of 86% and specificity of 80%. The study concluded that 18F-FDG combined with MRI can 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 in detecting changes in the acute and early late-onset phases of radiation brain injury, and SPECT and PET can image at the level of metabolic activity and have differential diagnostic value for late-onset radiation brain injury and tumor recurrence. 4. Treatment (1) Drugs: The initial treatment is based on cortisol, whose mechanism 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, usually with a long course, 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 protective effect and was most pronounced in the 100Gy 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. enzyme activity, reducing intra-membrane K+ efflux and Ca2+ inward flow, preventing membrane lipid hydrolysis, and blocking the cell membrane lipid peroxidation-radical cycle of free radicals, etc. (2) Hyperbaric oxygen: Hyperbaric oxygen can increase tissue oxygen partial pressure, stimulate endothelial growth factor production, and activate cellular and vascular repair mechanisms. 74 cases of hyperbaric oxygen treatment for radiation brain injury were analyzed by Feldmeier et al. Among them, 67 cases reported therapeutic or preventive effects, and cases not using hyperbaric oxygen often required surgical treatment. Thus, it is believed that hyperbaric oxygen can be used as a routine treatment for radiation brain injury and is 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 widespread cerebral edema and occupying effects are feasible for surgical treatment to remove necrotic tissue. When tumor recurrence and radiation brain necrosis are difficult to distinguish, and the occupying effect of the lesion is more obvious, the lesion should also be actively surgically removed.