title: Cortical reorganization after spinal cord injury: always for good?
abstract: Plasticity constitutes the basis of behavioral changes as a result of experience. It refers to neural network shaping and re-shaping at the global level and to synaptic contacts remodeling at the local level, either during learning or memory encoding, or as a result of acute or chronic pathological conditions. 'Plastic' brain reorganization after central nervous system lesions has a pivotal role in the recovery and rehabilitation of sensory and motor dysfunction, but can also be "maladaptive". Moreover, it is clear that brain reorganization is not a "static" phenomenon but rather a very dynamic process. Spinal cord injury immediately initiates a change in brain state and starts cortical reorganization. In the long term, the impact of injury - with or without accompanying therapy - on the brain is a complex balance between supraspinal reorganization and spinal recovery. The degree of cortical reorganization after spinal cord injury is highly variable, and can range from no reorganization (i.e. "silencing") to massive cortical remapping. This variability critically depends on the species, the age of the animal when the injury occurs, the time after the injury has occurred, and the behavioral activity and possible therapy regimes after the injury. We will briefly discuss these dependencies, trying to highlight their translational value. Overall, it is not only necessary to better understand how the brain can reorganize after injury with or without therapy, it is also necessary to clarify when and why brain reorganization can be either "good" or "bad" in terms of its clinical consequences. This information is critical in order to develop and optimize cost-effective therapies to maximize functional recovery while minimizing maladaptive states after spinal cord injury.
authors.affiliation: School of Biomedical Engineering, Science and Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, USA. Electronic address: Karen.Moxon@drexel.edu.
authors.forename: K A
authors.initials: KA
authors.lastname: Moxon
authors.affiliation: Hospital Nacional de Parapléjicos, SESCAM, Finca la Peraleda s/n, 45071 Toledo, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Oliviero
authors.affiliation: Hospital Nacional de Parapléjicos, SESCAM, Finca la Peraleda s/n, 45071 Toledo, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Aguilar
authors.affiliation: Hospital Nacional de Parapléjicos, SESCAM, Finca la Peraleda s/n, 45071 Toledo, Spain. Electronic address: gfoffani@sescam.jccm.es.
authors.forename: G
authors.initials: G
authors.lastname: Foffani
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology*; D006801:Humans; D007858:Learning / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology
keywords: brain plasticity; brain-derived neurotrophic factor; exercise; pain; serotonin; spinal transection