ONE of the outstanding characteristics of multiple sclerosis and other clinical and experimental diseases associated with demyelination, is the tendency to remit. Although there is good evidence that an important cause of functional loss in such conditions is conduction block produced by the selective destruction of the myelin sheath¹, the mechanisms underlying remission are unknown². It has long been recognised that in certain experimental lesions demyelinated central axons can be remyelinated by the normal myelin-forming cell, the oligodendrocyte³. The new sheaths are, however, abnormally thin and short and it is not known whether they are capable of restoring conduction. A previous investigation was inconclusive⁴. Because of the physiological and clinical importance of this problem, we have now examined conduction serially through the lesion induced by the direct microinjection of lysophosphatidyl choline (LPC) into the cat spinal cord⁵. This lesion has the advantage that the phases of active demyelination and remyelination are well separated, thus permitting a reasonable correlation of the morphological with the physiological changes. We have found that secure conduction is restored with remyelination.