Small volumes of ethidium bromide were injected into the dorsal columns of the spinal cord of Wistar rats. It was induced a demyelinating process, variable in nature and speed of repair according to the dose used. The induced lesions were classified into three groups (type I or fast lesions; type II or slow lesions; type III or intermediate lesions) according to the histological appearance and extension of remyelination. In some lesions or in areas within the same lesion, myelin and glial cell debris were rapidly processed by macrophages and the naked axons soon remyelinated by Schwann cells. In other lesions of similar duration, or areas within the lesions, myelin underwent transformation into mazes of membranes which persisted around the axons for long periods of time. In the lesions which contained such myelin_derived membranes, macrophages were scant and remyelination by Schwann cells was slow and arduous. It may be concluded that the slow resolution of some lesions resulted from the time elapsed between intoxication and disappearance of myelin_related cells. That time difference determined that the cellular responses to demyelination took place in an area devoid of glial cells and therefore without a support for the cellular migration needed for the removal of myelin debris and eventual remyelination. This investigation indicates that the development and outcome of demyelination may be altered by the cellular events that occur during oligodendrocyte degeneration.