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Hyperbaric Oxygen Therapy (HBOT) in Treatment of Cerebral Radiation Necrosis (CRN)

Cerebral radiation necrosis is borne from radiotherapy that is used to treat cancer and malignant growths in the brain. Necrosis results from long-term radiation exposure, and it has various adverse effects on the patients going through the condition. The condition mainly arises about 1-3 years after one is done with their radiation sessions. The earliest cases are diagnosed about six months after radiation treatment. Some of the most common forms of focal treatment that result in cerebral radiation necrosis include radioactive implants and stereotactic radiosurgery. Some of the common symptoms of the condition include headaches, cognitive decline, ataxia, seizures, and other focal neurologic defects such as cranial nerve palsy. The infarction, which involves obstruction of blood supply to the cerebral tissues, causes local tissue death. The infarction resulting from radiation-induced necrosis involves obstruction of blood supply to the cerebral tissues, causing local tissue death. Patients experience both vasogenic and cerebral edema as a result of a compromised blood-brain barrier. Lesions are cited quite often on the soft brain tissue as well. Some of the most explored forms of treatment for the condition include the use of corticosteroids, non-steroidal anti-inflammatory drugs, lipid peroxidase inhibitors, surgical management, anticoagulation therapy, and hyperbaric oxygen therapy (HBOT). The surgical methods include cutting off the avascular necrotic debris.

How HBOT Works

HBOT addresses the damage caused by radiation on the small and medium-sized blood vessels, thus increasing the supply of blood to the soft brain tissues. With time, the capillary, artery, and arteriole density and distribution around the irradiated tissues are able to go back to almost 100% normalcy. The increase in microvasculature also aids in faster recovery of the damaged cerebral tissues. The soft brain tissues can heal better as a result of angiogenesis and associated tissue perfusion. Chronic ischemia and coagulation, which lead to the death of cells, are also addressed through the increased tissue oxygenation in the cerebral region. HBOT also aids in getting rid of both vasogenic and cerebral edema which increase intracranial tissue pressure. Symptomatic and asymptomatic cerebral radiation necrosis are taken care of in the process. By boosting collagen synthesis, which is facilitated by fibroblasts, damaged tissue is replenished, which also leads to cognitive improvement. The endothelial cells are restored as the action of the vascular endothelial growth factor (VEGF) is blocked. HBOT also improves the efficiency of other forms of treatment, such as the use of steroids. In the severe stages, CRN is highly unresponsive to different types of treatment. However, with the introduction of a positive oxygen gradient, the functionality of other modes of treatment is improved as well. The patient is able to get back to normal functioning that had been affected initially. The performance status and quality of life are also improved.

References

Kohshi, K., Imada, H., Nomoto, S., Yamaguchi, R., Abe, H., & Yamamoto, H. (2003). Successful treatment of radiation-induced brain necrosis by hyperbaric oxygen therapy. Journal of the Neurological Sciences, 209(1–2), 115–117. https://doi.org/10.1016/s0022-510x(03)00007-8

Smith, J. A., & Fenderson, J. (2020). Diving into radiation necrosis: Hyperbaric oxygen therapy in cerebral radiation necrosis. JCO Oncology Practice, 16(8), 519–521. https://doi.org/10.1200/op.20.00058

 

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