The aim of this study is to review the previous experiments in order to identity future radiobiological research needed to elucidate the pathogenetic mechanisms of developing radiation myelopathy.Histopathological techniques were used to investigate the pathogenesis of radiation myelopathy. Interpretation of the pathogenesis of the spinal cord radiation injury pathogenesis was based, besides the assessment of functional injury mainly on morphological observations of histological specimens. In experimental models of radiation myelopathy, modern immuno-histochemical or immuno-enzymatic techniques have been used only sparsely that might convey functionally oriented information in addition to accurate definition of the various cells that participate in the evolutions of radiation myelopathy.Using paralysis as the endpoint, data from experiments with large fraction sizes, i.e. 19 Gy down to 2 Gy / fraction, were consistent with the linear quadratic (LQ) model and α/β value of 2.41 Gy. Data from experiments with small fraction sizes, i.e. 2 Gy down to 1 Gy/ fraction, however, gave a much smaller value of 0.48 Gy for */*. It reveals that the LQ model failed to provide a satisfactory description of the dose – fractionation response relationship in rat spinal cord.The change of fractionation sensitivity as doses per fraction are decreased suggests that at least two different types of target cells interact in the pathogenesis, each having different fractionation sensitivities. Recent in vitro clonogenic investigations in vitro or in vivo fractionated irradiation of adult rat glial progenitor cells revealed a much higher α/β value (4.9 – 7.3 Gy) for these stem cells, although this could be related to the proliferation state of these cells. Besides glial stem cells, vascular endothelial cell are candidates for primary target cell populations. In order to get a more comprehensive picture of the mechanisms of radiation effects in the spinal cord functional changes of endothelial cells in the spinal cord need to be studied.