Plasticity of motor systems after incomplete spinal cord injury

By O. Raineteau, Martin E. Schwab. Nature Reviews Neuroscience, 2001

828 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/cd40dfcc14abd722d2efe926e46dd3e89c2f3d4d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. M. Sofroniew
2. Y. Ao
3. B. Song
4. Jingwei Qi
5. J. Herrmann
6. Martin E. Schwab
7. Zhigang He
8. M. Pekny

In Neurology

1. M. Sofroniew
2. Y. Ao
3. B. Song
4. Jingwei Qi
5. J. Herrmann
6. Martin E. Schwab
7. J. Burda
8. M. Pekny

In Pathology and Forensic Medicine

1. M. Sofroniew
2. Martin E. Schwab

Citations in the corpus

• Nogo and axon regeneration. (2004, background): “Enhancing compensatory mechanisms in the injured CNS Even large spinal cord lesions that are partial can be followed by a considerable degree of functional recovery in humans and rats [56].”
• Recovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury (2008, background): “Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connection”
• Using human brain lesions to infer function: a relic from a past era in the fMRI age? (2004, background): “and also shows plasticity, with different regions changing their function in response to damage to one are”
• PTEN Deletion Enhances the Regenerative Ability of Adult Corticospinal Neurons (2010, background): “In principle, functional recovery after CNS injury could be achieved by two forms of axonal regrowth: sprouting of spared non-injured axons to form new circuits compensating for the lost functions and regeneration of lesioned axons that can potentially re-form the lost connection”