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Brain Advance Access originally published online on July 21, 2004
Brain 2004 127(10):2221-2231; doi:10.1093/brain/awh255
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Brain Vol. 127 No. 10 © Guarantors of Brain 2004; all rights reserved

Degradation of neuronal function following a spinal cord injury: mechanisms and countermeasures

Volker Dietz and Roland Müller

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

Correspondence to: Professor Dr Volker Dietz FRCP, Balgrist University Hospital, Spinal Cord Injury Center, Forchstrasse 340, 8008 Zurich, Switzerland E-mail: dietz{at}balgrist.unizh.ch

The aim of this study was to evaluate the course of spinal neuronal activity following spinal cord injury (SCI). In patients with a complete SCI, the leg muscle EMG activity early and up to 33 years after an SCI was analysed during locomotor movements induced and assisted by a driven gait orthosis (DGO). Only in chronic SCI patients did a premature exhaustion of neuronal activity occur. This was reflected in a reduced density and fading of leg muscle EMG activity. The early exhaustion of EMG activity was more pronounced in the leg flexor (e.g. biceps femoris) than extensor (e.g. gastrocnemius) muscles. The timing of the leg muscle pattern remained unchanged in the chronic patients. A preserved amplitude of motor action potentials following repetitive peripheral nerve stimulation and during spasms indicated an interneuronal site of impairment. In patients who participated in a locomotor training programme lasting up to 13 weeks, no positive effect on the slope of exhaustion was seen. It is concluded that a degradation of spinal neuronal activity takes place following an SCI. If in the future regeneration of spinal tract fibres becomes feasible in patients with complete SCI, such an approach can only become functionally successful if neuronal activity below the level of the lesion is maintained. This might be achieved by a continuous training approach starting early after injury.


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