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In addition, malfunctions such as neuropathic pain or muscle spasms develop in many patients, possibly caused by injury\u2010induced plastic changes of neuronal circuits above and below the lesion. New treatment strategies for spinal cord injury aim at enhancing plasticity and neurite growth, for example, by blocking the key neurite growth inhibitor Nogo\u2010A or its downstream effectors. It is therefore crucial to investigate potential effects of such treatments on malfunctions such as muscle spasms. In addition, locomotor training, now a standard therapeutic tool to improve walking ability in incomplete SCI subjects, can be expected to influence the rearrangement of spinal cord circuits and the development of muscle spasms and other malfunctions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and Results<\/jats:title><jats:p>Here we present and validate a new rat model for muscle spasms after incomplete SCI and show that both intrathecal anti\u2013Nogo\u2010A antibody treatment and locomotor training, started early after injury, permanently reduce the development of muscle spasms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>The results show that an antibody\u2010mediated suppression of the growth inhibitory protein Nogo\u2010A leads to functional recovery and a lower level of malfunctions, suggesting the formation of functionally meaningful connections in the damaged spinal cord. Treadmill training early after SCI also has a beneficial effect. 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