Neuronal dysfunction in chronic spinal cord injury.

[wildwilly]

Spinal Cord. 2010 Nov 9.

Neuronal dysfunction in chronic spinal cord injury.

Hubli M, Bolliger M, Dietz V.

Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland.

Abstract
This review describes the changes of spinal neuronal function that occur after a motor complete spinal cord injury (cSCI) in humans. In healthy subjects, polysynaptic spinal reflex (SR) evoked by non-noxious tibial nerve stimulation consists of an early SR component and rarely a late SR component. Soon after a cSCI, SR and locomotor activity are absent. After spinal shock; however, an early SR component re-appears 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, that is, 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 spinal cord injury (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. Training of spinal interneuronal circuits including the enhancement of an appropriate afferent input might serve as an intervention to prevent neuronal dysfunction after an SCI.Spinal Cord advance online publication, 9 November 2010; doi:10.1038/sc.2010.147.

http://www.ncbi.nlm.nih.gov/pubmed/21060314

[wildwilly]

Nat Rev Neurol. 2010 Mar;6(3):167-74.

Behavior of spinal neurons deprived of supraspinal input.

Dietz V.

Spinal Cord Injury Center, Balgrist University Hospital, Forchstrasse 340, 8008 Zürich, Switzerland. vdietz@paralab.balgrist.ch

Abstract
This Review discusses the spinal neuronal changes that occur after a complete spinal cord injury (SCI) in humans. Early after an SCI, neither locomotor nor spinal reflex activity can be evoked. Once spinal shock has resolved, locomotor activity and an early spinal reflex component reappear in response to appropriate peripheral afferent input. In the subsequent 4-8 months, clinical signs of spasticity appear, largely as a result of non-neuronal (for example, muscular) changes, whereas locomotor and spinal reflex activity undergo little change. At 9-12 months, the electromyographic amplitude in the leg muscles during assisted locomotion declines, accompanied by a decrease in the amplitude of the early spinal reflex component and an increase in the amplitude of a late spinal reflex component. This exhaustion of locomotor activity also occurs in nonambulatory patients with incomplete SCI. Neuronal dysfunction is fully established 1 year after the injury without further alterations in subsequent years. In chronic SCI, the absence of input from supraspinal sources has been suggested to lead to degradation of neuronal function below the level of the lesion or, alternatively, a predominance of inhibitory signaling to the locomotor pattern generator. Appropriate training and/or provision of afferent input to spinal neurons might help to prevent neuronal dysfunction in chronic SCI.

http://www.ncbi.nlm.nih.gov/pubmed/20101254