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  • Review Article
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Plasticity of motor systems after incomplete spinal cord injury

Nature Reviews Neuroscience volume 2, pages 263–273 (2001)Cite this article

Key Points

  • Functional recovery is observed in people with incomplete spinal cord injury, but the degree of recovery is variable. In addition to the cellular changes that occur at the lesion site, the central nervous system undergoes substantial reorganization that might occur at two levels: in pre-existing circuits by modifications of synaptic strength or by the appearance of new circuits through sprouting and anatomical reorganization.

  • The cerebral cortex can reorganize following peripheral damage. The mechanisms involved might include changes in the efficacy of cortical synapses, alterations in the degree of synaptic inhibition and anatomical changes such as the growth of axon arbours.

  • Subcortical structures also experience reorganization after spinal cord injury, as illustrated by the case of the red nucleus. The red nucleus can promote a certain degree of functional recovery after transections of the corticospinal tract. This recovery seems to be related to the anatomical plasticity of rubral afferents as well as the intrarubral circuitry.

  • Spinal pattern generators also show significant plasticity following lesions of the corticospinal tract. In fact, training can enhance functional recovery mediated by these pattern generators. This observation was made originally in animals, but the existence of spinal pattern generators in humans has led to the development of new therapeutic approaches to treat people with spinal cord injury. The mechanism that underlies pattern-generator-mediated recovery might involve an increase in spinal excitability or the formation of new circuits.

  • Descending motor pathways can anatomically reorganize to innervate novel targets. Their anatomical plasticity is influenced by myelin; specifically, by inhibitory proteins such as Nogo-A/NI-250, myelin-associated glycoprotein and proteoglycans. Similarly, the neurotrophic factors, as well as other molecules expressed during development, might be involved in process outgrowth after injury, but definitive evidence is missing.

Abstract

Although spontaneous regeneration of lesioned fibres is limited in the adult central nervous system, many people that suffer from incomplete spinal cord injuries show significant functional recovery. This recovery process can go on for several years after the injury and probably depends on the reorganization of circuits that have been spared by the lesion. Synaptic plasticity in pre-existing pathways and the formation of new circuits through collateral sprouting of lesioned and unlesioned fibres are important components of this recovery process. These reorganization processes might occur in cortical and subcortical motor centres, in the spinal cord below the lesion, and in the spared fibre tracts that connect these centres. Functional and anatomical evidence exists that spontaneous plasticity can be potentiated by activity, as well as by specific experimental manipulations. These studies prepare the way to a better understanding of rehabilitation treatments and to the development of new approaches to treat spinal cord injury.

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Figure 1: Organization of the motor cortex.
Figure 2: Electromyograph activity during bipedal hindlimb stepping in a step-trained and a non-trained cat before (–2 or –5 weeks) and 1, 4 and 12 weeks after spinalization.
Figure 3: Schematic representation of the corticospinal reorganization occurring after pyramidotomy and mAb IN-1 treatment.

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Acknowledgements

We would like to thank Karim Fouad and Florence Bareyre for critical reading of the manuscript. The Swiss National Science Foundation, the International Research Institute of Paraplegia (Zurich) and the Spinal Cord Consortium of the Christopher Reeve Paralysis Fundation (Springfield, New Jersey) supported this work.

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Authors and Affiliations

  1. Brain Research Institute, University and ETH Zurich , Winterthurerstrasse 190, Zurich , 8057, Switzerland

    Olivier Raineteau & Martin E. Schwab

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  1. Olivier Raineteau
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Related links

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DATABASE LINKS

Nogo-A

glutamate decarboxylase

GAP-43

MAG

brevican

versican

NT-4/5

BDNF

NT-3

TRkB

TrkC

semaphorin 3A

EphB3

ENCYCLOPEDIA OF LIFE SCIENCES

Traumatic central nervous system injury

Motor neurons and spinal control of movement

Motor output from the brain and spinal cord

Nerve regeneration: mammalian

Glossary

SPASTICITY

Persistent contraction of certain muscles, which causes stiffness and interferes with gait, movement or speech.

VASOGENIC OEDEMA

Accumulation of extracellular fluid that results from changes in capillary permeability, allowing for the seepage of plasma molecules and water.

TRANSCRANIAL MAGNETIC STIMULATION

A technique use to induce a transient interrruption of normal brain activity in a restricted area of the brain. It is based on the generation of a strong magnetic field near the area of interest which, if changed rapidly enough, will induce an electric field sufficient to stimulate neurons.

LONG-TERM POTENTIATION AND DEPRESSION

Long-lasting activity-dependent changes in the efficacy of synaptic transmission.

RED NUCLEUS

Midbrain structure that receives motor information from the deep cerebellar nuclei and projects to higher motor centres, as well as to the spinal cord (rubrospinal tract).

CENTRAL PATTERN GENERATOR

Neural circuits that produce self-sustaining patterns of behaviour independently of their sensory input.

SUBSTANTIA GELATINOSA

Layer of the dorsal horn in the spinal cord in which sensory afferents form synapses with nociceptive neurons of the anterolateral system.

DNA MICROARRAY

Devices used to interrogate complex nucleic acid samples by hybridization. They make it possible to count the number of different RNA or cDNA molecules that are present in the sample of interest as a preparative stage for their subsequent characterization.

DORSAL RHIZOTOMY

Selective transection of the dorsal nerve root. It is performed to reduce nociceptive perception in the affected area while sparing motor function.

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Raineteau, O., Schwab, M. Plasticity of motor systems after incomplete spinal cord injury. Nat Rev Neurosci 2, 263–273 (2001). https://doi.org/10.1038/35067570

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