In this issue of Spinal Cord, several important studies and reviews are presented.
Hubli et al. describe the changes of spinal neuronal function that occur after a motor complete spinal cord injury (cSCI) in humans. Early after a cSCI, spinal reflex (SR) and locomotor activity are absent. After spinal shock, an early SR component reappears associated with the recovery of locomotor activity in response to appropriate peripheral afferent input. Clinical signs of spasticity take place in the following months, largely as a result of non-neuronal changes. After around 1 year the locomotor and SR activity undergo fundamental changes, i.e. the electromyographic amplitude in the leg muscles during assisted locomotion exhaust rapidly, accompanied by a shift from early to dominant late SR components. The exhaustion of locomotor activity is also observed in non-ambulatory patients with an incomplete SCI. At about 1 year after injury in most cSCI subjects the neuronal dysfunction is fully established and remains more or less stable in the following years. It is assumed that in chronic SCI the patient's immobility resulting in a reduced input from supraspinal and peripheral sources leads to a predominance of inhibitory drive within spinal neuronal circuitries underlying locomotor pattern and SR generation. The authors suggest that training of spinal interneuronal circuits including the enhancement of an appropriate afferent input might serve as an intervention to prevent neuronal dysfunction after SCI.
