Late radiation damage to the central nervous system: a radiobiological interpretation.
The evidence in support of the two opposing views as to the pathogenesis of late radiation damage to the central nervous system after therapeutic doses of radiation are briefly reviewed. Analysis of the radiation dose levels used by various investigators holding opposing views as to pathogenesis of CNS lesions they reported, suggests that both groups of protagonists were in part correct. Both vascular and glial changes are important in the development of late radiation damage to the nervous system; the preponderance of one or the other type of cell damage depends upon the radiation dose. Vascular effects occur at lower dose levels but after a longer latent period than effects mediated through damage to neuroglia. Current radiobiological concepts and their possible importance in establishing the radiosensitivity of the central nervous system are discussed. The origins of both vascular and neuroglial cell mediated changes are discussed in terms of the reproductive loss of radiation damaged cells. This view is supported by some recent experimental findings. The radiobiological basis of some recently investigated treatment modalities aimed at improving the control of intracranial gliomata by radiotherapy are also considered.
D000818:Animals; D001921:Brain / Q000473:pathology / Q000528:radiation effects*; D002470:Cell Survival / Q000528:radiation effects; D004307:Dose-Response Relationship, Radiation; D006801:Humans; D011832:Radiation Injuries / Q000473:pathology; D013116:Spinal Cord / Q000528:radiation effects*