| Abstract No.: | 213 |
| Country: | Canada |
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| Title: | Plasticity Induced After Spinal Cord Injury by Treadmill Locomotor Training |
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| Authors/Affiliations: | S. Rossignol*, G. Barrière and A. Frigon
Groupe de recherché sur le Système Nerveux Central (GRSNC of the FRSQ), Department of Physiology, Faculty of Medicine, Université de Montréal, QC, Canada
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| Content: | Locomotion is controlled by different interacting structures of the nervous system. At the core is an innate central pattern generator (CPG), located in the spinal cord, capable of producing the complex sequence of muscle activation typical of locomotion. The spinal CPG is continuously updated by afferent information generated by the muscles, joints and skin of the walking limbs. Descending pathways from the brainstem can adjust the general level of excitability of the CPG through neurochemical modulation but can also correct the locomotor pattern on an ongoing basis. Cortical control not only starts and stops the pattern but can also modify it, to overcome obstacles for example. The CPG, afferent inputs and descending control are normally in an exquisite balance. However, this balance can be perturbed by various types of peripheral and/or central lesions and a new state of equilibrium within the spinal locomotor circuitry is reached, which suggests important plastic mechanisms within the spinal cord. After a complete spinal section at the last thoracic segment (T13), adult cats can regain spontaneous hindlimb locomotion on a treadmill after weeks of locomotor training, which is accompanied by modified transmission in various reflex pathways. This implies that the CPG can function without descending signals and that peripheral inputs, strengthened by locomotor training, play a significant role in the recovery of locomotion. The situation is less clear with partial spinal cord injury (SCI) in which some sensory-motor functions are preserved while others are lost, at least in the acute period after the lesion. A remarkable finding however, from animal experiments and observations in humans, is that there can be remarkable recovery of some functions with time after partial spinal cord injury (SCI). Although this might be due to sprouting of undamaged pathways or regeneration plastic changes below the lesion within spinal circuits could also be involved. One can indeed ask to what extent is the spinal CPG involved in the recovery of locomotion after partial SCI? We devised a dual lesion paradigm where a unilateral partial spinal lesion was initially made at T10-11 and following a period of treadmill training to facilitate locomotor recovery a second but complete spinal section was performed at T13. We hypothesized that changes intrinsic to the spinal cord occurring during the period of locomotor recovery after the partial lesion could be retained and demonstrated early after the complete section. Our major finding was that treadmill-trained cats walked remarkably well with the hindlimbs within 24 hours (i.e. the first testing session) following the complete spinal section. Therefore, although both supraspinal and spinal mechanisms are involved in the recovery of voluntary goal-oriented locomotion after partial SCI, the present experiments show a major functional contribution by the spinal cord. Such neuroplasticity should be targeted in rehabilitation strategies to reinforce voluntary aspects of locomotion and the endogenous spinal circuitry in humans with SCI
Supported by the Multidisciplinary Locomotor Rehabilitation Team after spinal cord injury and stroke (CIHR Strategic Initiative in Regenerative Medicine), a Canada Research Chair on the Spinal Cord, individual and group grants from CIHR, fellowships from FRSQ (G.B.) and NSERC and GRSNC (A.F).
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