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Published on: October 18, 2011
Pathobiology of radiation myelopathy and strategies to mitigate injury
C S Wong1, M G Fehlings2, A Sahgal3
1Department of Radiation Oncology, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada.
Study Design:
This is a narrative review of the literature.
Objectives:
The objectives of this study were to review the current concepts underlying the pathobiology of radiation-induced spinal cord injury; to discuss potential biologic strategies to mitigate spinal cord injury following radiation; and to provide an update on the clinical guidelines to prevent injury in the era of image-guided stereotactic body radiotherapy (SBRT).
Setting:
This study was conducted in Toronto, Canada.
Methods:
A MEDLINE search was performed using the following terms: radiation injury; radiation myelopathy; CNS radiation injury; brain necrosis, radiation; demyelination, radiation; blood-brain barrier, radiation; white matter necrosis; and SBRT.
Results And Conclusion:
The biologic response of the spinal cord after radiation is a continuously evolving process. Death of vascular endothelial cells and disruption of the blood-spinal cord barrier leads to a complex injury response, resulting in demyelination and tissue necrosis. At present, there is no evidence that the pathobiology of cord injury after SBRT is different from that after standard fractionation. Although permanent myelopathy has become a rare complication following conventional fractionated radiation treatment, cases of radiation myelopathy have re-emerged with the increasing role of spine stereotactic body radiation therapy and reirradiation. Experimental biologic strategies targeting the injury response pathways hold promise in mitigating this dreaded late effect of radiation treatment.
