Radiotherapy (RT) is a feasible therapeutic option applied in central nervous system malignant lesions as an adjuvant therapy.1 Radiation necrosis (RN) or adverse radiation effect develops as a late complication of RT of the intracranial lesions.2,3 RN is generally defined as a severe local tissue reaction that frequently develops 3–12 months after RT; however, RN may develop years after RT.4 The incidence of RT is increasing worldwide due to escalation in the application of stereotactic radiosurgery (SRS).2,4 The first case of cerebral RN was reported in a 45-year-old male in 1930 following irradiation to the scalp.5 The precise underlying pathophysiology of RN remains unclear; however, it has been suggested that vascular alteration due to endothelial injury and proinflammatory cytokines, including vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1, and tumor necrosis factor α (TNF-α), play an important role.6 Several factors may predispose the patient to develop RN, including RT dose, prior whole brain RT, concurrent systemic administration of chemotherapeutic agents, cancer subtype, and size of the primary lesion.6 The radiologic differentiation of RN and tumor reoccurrence is challenging.6 Advanced imaging modalities may aid physicians in differentiating between these 2 conditions; however, histopathological examination is the gold standard diagnostic intervention.6 The first-line treatment for asymptomatic or small-size RNs is close observation.6 In symptomatic patients, a course of glucocorticoids is the first-line therapeutic option, and in contrast to tumor reoccurrence, rapid symptom relief is expected in RN cases following the administration of steroids.6 In those who fail to respond to glucocorticoids or are intolerant of glucocorticoids, several therapeutic options are available.6 These options include bevacizumab, laser interstitial thermal therapy, surgery, and hyperbaric oxygen therapy (HBOT).6

HBOT is mainly known for managing infectious and decompression sickness; however, HBOT has been applied in several cerebral conditions, including stroke, spinal cord trauma, intracranial infections, and edema.7 Nowadays, HBOT is applied concurrent with RT or chemotherapy as an adjuvant therapeutic option in managing brain tumors.8 In HBOT, a patient is positioned in a chamber and breaths pressurized oxygen that elevates blood oxygen levels and enhances the cellular repair mechanism.7 Consequently, oxygen delivery is amplified to the affected tissue, resulting in stimulation of angiogenesis and neovascularization; therefore, the blood supply is increased, and consequently, the healing process is promoted.7 Previous studies investigated the utilization of HBOT in the treatment of intracranial RNs.7, 8, 9, 10 In most cases, HBOT was feasible and associated with favorable outcomes with few side effects.1,8,9,11,12

In this review article, we aimed to discuss the pathophysiology of RN, HBOT structure, clinical application of HBOT in intracranial RN, and limitations of HBOT.