Spinal cord trauma causes lack of communication between complex processor systems (brain) and the conducting system (spinal cord). After spinal cord trauma, the main problem is injury to the white matter. Disability of motor functions and paralysis after spinal cord injury (SCI) are primarily caused by axonal injuries or dysfunction in the white matter. One necessary element of recovery in post-traumatic spinal cord is long tract axonal regeneration. The ultimate goal of spinal cord regeneration research is to restore motor and sensory function in individuals that have lost these capabilities due to disease or injury. The mammalian central nervous system shows plasticity due to synaptic reorganization and axon branching. After nerve injury, dense regeneration of central axons begins and the microenvironment at the tip of the axon organizes this regenerative response. Inhibitor effects of this microenvironment soon stop the initial regeneration attempt. If the environment of the axon of the mammalian spinal cord is modified with drugs, cell transplant, cell graft, and various tropic factors, these axons may be stimulated to regenerate. In order to demonstrate spinal cord regeneration following axonal disconnection, 1) anatomic evidence of axonal regeneration, 2) electrophysiological evidence of functional synapses and 3) clinical evidence of functional recovery should be demonstrated. Following spinal cord trauma, recovery of neurological functions may be achieved by the existence and transplanting of stem cells which have the ability to migrate and multiply in the spinal cord, bridging the injured area with nerve grafts and applying exogenous growth factors to the spinal cord. On the basis of the results of animal studies, it may be stated that effective regenerative treatment of spinal cord injury is not speculation, but a realistic target.