Recovery from spinal cord injury: regeneration, plasticity and rehabilitation

Experimental spinal cord injury is no longer incurable. Many papers have appeared over the past few years reporting functional recovery following a variety of treatments. These have included interventions that affect myelin inhibitory molecules and their receptors, or inhibitory chondroitin sulphate proteoglycans, and treatments in which the regenerative potential of axons has been stimulated through growth-factor receptors or manipulation of internal signalling pathways (for reviews see Buchli and Schwab, 2005; Fawcett, 2006; Hannila et al. , 2007). There has also been success with strategies that bridge the injury using various axon growth-promoting cell types (Fouad et al. , 2005; Biernaskie et al. , 2007; Raisman and Li, 2007). Functional recovery has been seen in hindlimbs and forelimbs and affecting walking, skilled movements, sensation and other outcome measures. This is all very encouraging, but it is still not entirely clear what changes are responsible for the recovery. Many of the successful treatments stimulate axon regeneration through the site of injury, but most also stimulate plasticity. In the field, plasticity is used as a term to describe short-distance sprouting above and below the lesion and changes in synaptic strength, together enabling the CNS to change its connectivity. Thus, treatments that affect NogoA signalling and chondroitin sulphate proteoglycans, in addition to stimulating spinal cord axon regeneration, also promote reactivation of ocular dominance, the most studied example of plasticity (Pizzorusso et al. , 2002; McGee et al. , 2005). Is functional return in the injured cord due to the small number of axons that regenerate, or due to plasticity in …