Spinal neuronal dysfunction after deprivation of supraspinal input

Abstract

A central nervous system lesion can lead to remote structural and functional changes which may limit functional recovery. For example, after a spinal cord injury (SCI) structural and functional alterations of spinal neuronal networks take place: in the first weeks after an SCI, neither locomotor nor spinal reflex (SR) activity can be evoked. Once spinal shock has resolved, an early SR component can be re-evoked and locomotor electromyography (EMG) activity re-appears when appropriate proprioceptive input is provided. In a more chronic stage of SCI alterations in SR components are accompanied by a decline of EMG amplitude in the leg muscles during assisted locomotion. According to rodent experiments it is assumed that the deprivation of supraspinal input and the lack of meaningful proprioceptive input to spinal neuronal networks account for such alterations. A critical combination of sensory cues through physiological training strategies might prevent the development of an undirected neural plasticity.