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  • Review Article
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Behavior of spinal neurons deprived of supraspinal input

Nature Reviews Neurology volume 6, pages 167–174 (2010)Cite this article

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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.

Key Points

  • After spinal cord injury (SCI), spinal neuronal circuits deprived of supraspinal input undergo profound changes in their behavior, which are reflected in impairment of both locomotor activity and associated reflexes

  • Neuronal dysfunction after severe SCI becomes established over a 1 year period, and leads to an early exhaustion of locomotor electromyographic activity during assisted stepping

  • After severe SCI, spinal reflexes associated with locomotor activity shift from an early spinal reflex component (also present in healthy individuals) to the dominance of a late reflex component

  • Immobility after an SCI, with the loss of afferent input to spinal locomotor centers, leads to weakened function of excitatory neuronal circuits underlying locomotor and reflex activity

  • Severe SCI is followed by an imbalance in the activity of excitatory and inhibitory neuronal circuits that normally shape the locomotor pattern

  • Adequate animal models exist only for the early stages of deprivation of supraspinal input; chronic animal models are required to define the neuronal dysfunction more precisely and develop appropriate countermeasures

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Figure 1: Electromyographic recordings of spinal reflex responses and locomotor activity.
Figure 2: Behavior of spinal neuronal circuits that control locomotion and spinal reflexes.

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Acknowledgements

I would like to thank Professors B. Gähwiler and Y. von Cramon for helpful comments and discussions, and R. Jurd for editorial assistance. This work was supported by the Seventh Framework Program of the European Commission (project 'Spinal Cord Repair'; HEALTH-F2-2007-201144) and the Swiss National Research Foundation (320030-117768).

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  1. Spinal Cord Injury Center, Balgrist University Hospital, Forchstrasse 340, Zürich, 8008, Switzerland

    Volker Dietz

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Dietz, V. Behavior of spinal neurons deprived of supraspinal input. Nat Rev Neurol 6, 167–174 (2010). https://doi.org/10.1038/nrneurol.2009.227

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