Comment on the recent results of Hopewell, Morris and Dixon-Brown on radiation myelitis produced by irradiation of very short segments of rat spinal cord

Abstract

Recently, we proposed a model for radiation damage to normal tissue (Yaes & Kalend, 1988), based on the assumption that, because of the limited mobility and reproductive capacity of stem cells (Hellmann & Botnick, 1977) in adult mammalian organs, for each organ there is a maximum volume, which we have called the “critical volume”, that can be repopulated and repaired by a single surviving stem cell. When a critical volume is totally depleted of stem cells, irreparable damage results; however, a single surviving stem cell within the critical volume prevents the damage from occurring. These assumptions constitute the “local stem cell depletion hypothesis” (Yaes & Kalend, 1988). For the spinal cord, we represent the critical volume as a transverse “slice” of thickness t, assumed to be small compared with lengths of spinal cord usually irradiated clinically. If irreparable damage occurs to a single slice, the long motor and sensory tracts passing through it would be damaged, giving rise to radiation myelitis.