Promoting anatomical plasticity and recovery of function after traumatic injury to the central or peripheral nervous system

Traumatic brain or spinal cord injury (SCI) has devastating consequences for patients, and can lead to life-long disability. However, even in the most serious cases, there is normally some recovery of function. For example, 73% of patients who initially present with complete paralysis but sacral sensory sparing recover some motor function within a year (Marino et al ., 1999). The mechanisms of this recovery are still poorly understood and are likely to include the following: reduction of local ischaemia, oedema and inflammation; recovery from spinal shock of traumatized but undamaged pathways; remyelination of demyelinated axons; functional synaptic plasticity allowing spared pathways to take over the lost functions; and anatomical plasticity leading to new, and functionally effective, circuitry. In the past few years it has become apparent that the last of these possibilities, anatomical plasticity, may play a significant role. Although the CNS is not able to regenerate a major pathway such as the corticospinal tract, there is accumulating evidence that some pathways are able to sprout locally to establish novel circuits that restore a limited degree of function. The key question is, can such plasticity be promoted to enable patients to recover complex functions such as fine hand control? This exciting possibility is addressed by two papers in this issue of Brain from James Fawcett and colleagues at the Cambridge Centre for Brain Repair (Galtrey et al ., 2007; Smith et al ., 2007).After injury to a pathway such as the corticospinal tract, axons normally die back a short distance but then initiate a regenerative response which is unsuccessful and confined to local sprouts at the injury site (Kerschensteiner et al ., 2005). However recent studies have demonstrated that both damaged and undamaged pathways distant from the injury site can sprout to establish functional connections (Raineteau and …