Early treatment of spinal cord lesions is undertaken following two lines of research carried in adult rats: First, the reduction of secondary lesions, immediately after the trauma, second, the prevention of glial scar formation in the following days. In the first case, after a photochemical focal lesion at thoracic level (T8), a specific, non competitive antagonist of NMDA, TCP, is injected systemically. The result is the reduction of the extent of the lesion, as measured in serial coronal sections, the improvement of the performance in two functional tests of hindlimb function, and the improvement of somatosensory evoked potentials. In the second case, the spinal cord of rats were hemisected at thoracic level (T8-T9), and a suspension of liposomes containing a cholesterol derivative (7 beta-OH cholesteryl-oleate) was administered through a sub dural catheter, 2 days after the section. Histological investigations evidenced a reduction of astrocyte hyperplasia and hypertrophy, together with the blocking of the expression of a cell adhesion molecule, the so-called polysialic N-CAM. This resulted, within 5 weeks after the lesion, in the growth of axons in the denervated dorsal horn, below hemisection originating from the contralateral side. In conclusion, these two experimental studies constitute the basis for a coherent strategy of treatment in spinal cord traumatic lesions. Their sequential application could even improve the functional outcome of spinal cord lesions. However, these two research lines do not exclude other associated treatments such as the local applications of growth factors, which can potentiate both neuron survival and axonal sprouting.