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Changes in spinal reflex and locomotor activity after a complete spinal cord injury: a common mechanism?

Dietz, V. ; Grillner, S. ; Trepp, A. ; Hubli, M. ; Bolliger, M.

In: Brain, 2009, vol. 132, no. 8, p. 2196-2205

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    Titre
    • Changes in spinal reflex and locomotor activity after a complete spinal cord injury: a common mechanism?
    Auteur
    • Dietz, V.. 1 Spinal Cord Injury Centre, University Hospital Balgrist, Zurich, Switzerland
    • Grillner, S.. 2 Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institute, Stockholm, Sweden
    • Trepp, A.. 1 Spinal Cord Injury Centre, University Hospital Balgrist, Zurich, Switzerland
    • Hubli, M.. 1 Spinal Cord Injury Centre, University Hospital Balgrist, Zurich, Switzerland
    • Bolliger, M.. 1 Spinal Cord Injury Centre, University Hospital Balgrist, Zurich, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Brain, 2009, vol. 132, no. 8, p. 2196-2205. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:299279
    Summary
    Locomotor activity and spinal reflexes (SRs) show common features in different mammals, including humans. Here we report the time-course of the development of locomotor activity and SRs after a complete spinal cord injury in humans. SRs evoked by tibial nerve stimulation were studied, as was the leg muscle electromyography activity evoked by mechanically assisted locomotion (Lokomat) in biceps femoris, rectus femoris, tibialis anterior and gastrocenmius medialis. Around 8 weeks after the injury, an early SR component (latency 60-120 ms) appeared, as in healthy subjects, and a well-organized leg muscle activity was present during assisted locomotion. At around 6 months after injury an additional, late reflex component (latency 120-450 ms) appeared, which remained even 15 years after the spinal cord injury. In contrast, the early component had markedly decreased at 18 months after injury. These changes in SR were associated with a loss of electromyography activity and a successively stronger electromyography exhaustion (i.e. decline of electromyography amplitude), when comparing the level of electromyography activity at 2 and 10 min, respectively, during assisted locomotion. These changes in electromyography activity affected mainly the biceps femoris, gastrocenmius medialis and tibialis anterior but less so the rectus femoris. When the amplitude relationship of the early to late SR component was calculated, there was a temporal relationship between the decrease of the early component and an increase of the late component and the degree of exhaustion of locomotor activity. In chronic, severely affected but sensori-motor incomplete spinal cord injury subjects a late SR component, associated with an electromyography exhaustion, was present in subjects who did not regularly perform stepping movements. Our data are consistent with the proposal of a common mechanism underlying the changes in SR activity and locomotor activity after spinal cord injury. These findings should be taken into consideration in the development of novel rehabilitation schemes and programs to facilitate regeneration-inducing therapies in spinal cord injury subjects