In stroke, spinal cord injury, and cerebral palsy there is denervation of target neuron centers, which are self-organizing maps (SOMs) within the neuraxis. Compensatory reinnervation occurs within those SOMs by acquiring synaptic sprouts from whatever neurons in the neighborhood. Such reorganizations are more often maladaptive than beneficial. Motor recovery, if any appears, is incomplete and compromised. Cognitive systems studies indicate that motor paralysis is due to loss of learning <--> recall balance in those compensated SOMs, which had been locked into a stability <--> plasticity dilemma. Treatment/rehabilitation should aim therefore to first restore this learning related balance. The use of botulinum toxin as a neuromotor relearning tool to improve motor recovery is discussed.

In adult life a severe injury of the spinal cord results in total loss of locomotor functions of the hind limbs, i.e., paraplegia. However, after similar injury in neonatal life most hind limb functions are retained unaffected into adult life. Can such survival of locomotor function be produced in an adult paraplegic? Observations based on our previous studies suggest that sparing of function in the neonate is due to: 1) incomplete development of descending cord tracts 2) the presence of polyneuronal control of limb muscles by spinal motoneurons and 3) active growth of synaptic connections occurring in the cord while limbs are polyneuronally innervated. Such growth and remodelling ceases once mononeuronal (= adult) control of limb muscles is established. We suggest that recreation of conditions similar to neonatal life would be able to revive lost locomotor functions in the adult paraplegic. Experimental animal models are outlined here which may form a basis for future research.