A lesão medular (LM) promove uma condição devastadora que resulta em déficits sensorial e motor, impedindo o desempenho funcional do indivíduo. Modelos experimentais de lesão medular têm sido utilizados na investigação do funcionamento do sistema sensório-motor e da reorganização promovida por meio de tratamentos, podendo corroborar com aplicações clínicas atuais e futuras. Este trabalho tem como objetivos verificar a recuperação funcional e a dinâmica da reorganização cortical do sistema sensório-motor de ratos Wistar lesados medulares submetidos a treinamento motor. 17 ratos foram divididos aleatoriamente em três grupos: treinado (n = 6), controle (n = 7) e sham (n = 4). Todos os animais receberam um implante de matriz de 32 micro-elétrodos no córtex sensório-motor. Os animais do grupo treinado e controle foram submetidos à LM contusa e os do grupo sham somente ao procedimento cirúrgico sem a LM. Foram realizadas as avaliações comportamentais motoras, de dor neuropática (alodínea e hiperalgesia mecânica), de dor térmica e eletrofisiológica antes da LM e nos 1º, 3º, 5º, 7º, 14º, 21º, 28º, 35º, 42º, 49º e 56º dias pós-operatórios (dPO) da lesão. O grupo treinado realizou treinamento motor em uma esteira com velocidade controlada, tendo início no 5º dPO e foi realizado por 15 minutos, cinco vezes na semana até o final do experimento. Os outros dois grupos ficaram sem treinamento. No 57º dPO, os animais foram sacrificados, e as medulas espinhais e os encéfalos foram coletados para análise histológica. Os resultados mostraram melhora motora significativa do grupo treinado em relação ao controle. Ao final do experimento, os animais treinados foram capazes de realizar passos plantares coordenados consistentes de forma independente. Ambos os grupos lesados apresentaram alodínea após a LM, mas somente o controle apresentou aumento da dor mecânica. Os dados eletrofisiológicos revelaram alterações na atividade cortical sensório-motora no 1º dPO e ao longo do tempo. Foi identificado que o aumento da potência da banda beta contribuiu para a melhora motora do grupo treinado e o aumento da potência delta contribuiu para a recuperação motora limitada do grupo controle. Na análise histológica os grupos não diferiram em relação ao tamanho da lesão, mas foi identificada uma diminuição significativa dos neurônios do corno ventral da medula espinhal, no segmento caudal à lesão para os animais controles. O treinamento na esteira potencializou a recuperação funcional e parece ter facilitado a reorganização do córtex sensório-motor após a lesão. Esses resultados podem servir de base para futuras aplicações clínicas em pacientes lesados medulares / Spinal cord injury (SCI) results in a devastating condition, which leads to motor and sensory deficits that impair the injured person functional performance. Spinal cord injury experimental models are used in sensory-motor functioning and reorganization or plasticity promoted by trainings investigation. Thus, these studies can corroborate with current and future clinical approaches. This work aims to verify the functional recovery and the sensorimotor cortical reorganization dynamics in Wistar rats with spinal cord injury submitted to motor training. 17 rats were randomly divided into 3 groups: trained (n = 6), control (n = 7) and sham (n = 4). All animals received a 32 microelectrodes array in the sensorimotor cortex. Control and trained animals were submitted to contusive SCI and the sham group only to the surgical procedure without the contusion. Motor behavior, neuropathic pain (allodynia and mechanical hyperalgesia), thermal pain and electrophysiological assessments were accomplished before SCI and on the 1st, 3rd, 5th, 7th, 14th, 21st, 28th, 35th, 42nd, 49th and 56th post-operative days (POd). The trained group performed the motor training on a treadmill with controlled speed, starting on the 5th post-operative day and it was done for 15 minutes, five times per week till the end of the experiment. The other two groups did not receive any training. Soon after SCI the animals completely lost the hindlimbs movements. On the 57th POd, the animals were sacrificed and the spinal cords and brains were collected for histological analysis. Results showed significant motor improvement of the trained group. In the end of the experiment, these animals were able to perform consistent coordinated plantar steps on their own. Both injured groups showed allodynia after the SCI, but only the control group presented increased mechanical pain. Electrophysiological data revealed sensorimotor cortical activity changes on the 1st POd and over time. It was indentified that an increase in beta power contributed to the trained group motor improvement and that an increase in delta power contributed to the limited motor recovery of the control group. In the histological analysis the groups did not differ concerning the lesion size, but a significant spinal cord ventral horn neurons decrease in the lesion caudal segment compared to the controlled animals was identified. The treadmill training enhanced functional recovery and seemed to facilitate sensorimotor reorganization after injury. These results can be applied for future clinical interventions in spinal cord injured patients. Spinal cord injury (SCI) results in a devastating condition, which leads to motor and sensory deficits that impair the injured person functional performance. Spinal cord injury experimental models are used in sensory-motor functioning and reorganization or plasticity promoted by trainings investigation. Thus, these studies can corroborate with current and future clinical approaches. This work aims to verify the functional recovery and the sensorimotor cortical reorganization dynamics in Wistar rats with spinal cord injury submitted to motor training. 17 rats were randomly divided into 3 groups: trained (n = 6), control (n = 7) and sham (n = 4). All animals received a 32 microelectrodes array in the sensorimotor cortex. Control and trained animals were submitted to contusive SCI and the sham group only to the surgical procedure without the contusion. Motor behavior, neuropathic pain (allodynia and mechanical hyperalgesia), thermal pain and electrophysiological assessments were accomplished before SCI and on the 1st, 3rd, 5th, 7th, 14th, 21st, 28th, 35th, 42nd, 49th and 56th post-operative days (POd). The trained group performed the motor training on a treadmill with controlled speed, starting on the 5th post-operative day and it was done for 15 minutes, five times per week till the end of the experiment. The other two groups did not receive any training. Soon after SCI the animals completely lost the hindlimbs movements. On the 57th POd, the animals were sacrificed and the spinal cords and brains were collected for histological analysis. Results showed significant motor improvement of the trained group. In the end of the experiment, these animals were able to perform consistent coordinated plantar steps on their own. Both injured groups showed allodynia after the SCI, but only the control group presented increased mechanical pain. Electrophysiological data revealed sensorimotor cortical activity changes on the 1st POd and over time. It was indentified that an increase in beta power contributed to the trained group motor improvement and that an increase in delta power contributed to the limited motor recovery of the control group. In the histological analysis the groups did not differ concerning the lesion size, but a significant spinal cord ventral horn neurons decrease in the lesion caudal segment compared to the controlled animals was identified. The treadmill training enhanced functional recovery and seemed to facilitate sensorimotor reorganization after injury. These results can be applied for future clinical interventions in spinal cord injured patients

Introduction : L'Accident Vasculaire Cérébral (AVC) est la 1ère cause de handicap acquis chez l'adulte, dans les pays industrialisés. 20% des patients décèdent dans le mois qui suit, 75% des survivants gardent des séquelles définitives, 33% deviennent dépendant à vie. Il n'existe pour l'heure aucune thérapie de récupération quand les déficits fonctionnels sont en place hormis la rééducation. Chez l'homme, 80% des AVC thrombotiques touchent l'artère cérébrale moyenne, qui irrigue le cortex moteur primaire (M1). M1 projette des axones jusque dans la moelle épinière et forme le Faisceau Cortico Spinal (FCS). Après une atteinte de M1, ce faisceau dégénère et cela induit des déficits fonctionnels de force et de dextérité. M1 est indispensable pour les mouvements volontaires dextres garants de l'indépendance du patient. Objectif : Mise au point d'un modèle de lésion cérébrale, chez un primate non humain, le marmouset, qui permette d'évaluer la récupération fonctionnelle motrice afin d'étudier l'effet de neuro-implants. Méthode : 14 marmousets ont servi à caractériser le nouveau modèle lésionnel induit par une injection stéréotaxique d'une toxine inhibant le métabolisme cellulaire. Des tests comportementaux, évaluant le score neurologique, la dextérité et la force de traction du membre supérieur, ont permis d'évaluer la récupération fonctionnelle en phase aiguë, subaiguë et chronique jusqu'à 6 mois après la lésion. Le suivi longitudinal structural et fonctionnel de la lésion et de la récupération a été réalisé par IRM (T1, T2, DTI). Le suivi de l'intégrité du FCS a été étudié, pour la première fois chez le marmouset, grâce à une technique (ME-MRI, manganese-enhanced-MRI) utilisant un agent de contraste injecté directement dans le cortex M1, capté par les neurones et traçant les voies neuronales. Une étude pilote sur 3 marmousets a testé l'effet de neuro-implants microstructurés dans la lésion cérébrale associés à l'injection de chondroïtinase ABC (enzyme de dégradation de la matrice extracellulaire). / Introduction: Stroke is the first leading cause of acquired handicap and disability in adults in industrialized countries. 20% of patients die in the following month, 75% of survivors remain with definitive sequelae, 33% become dependent for life. No therapy in the recovery phase exists today when functional deficits are installed except rehabilitation. In human, 80% of thrombotic stroke affect middle cerebral artery, which supplies the primary motor cortex (M1). M1 projects axons to the spinal cord and forms the CorticoSpinal Tract (CST). After an M1 insult, this tract degenerates and functional deficits of force and dexterity are induced. M1 is essential for voluntary dexterous movements that make patients independent. Objective: Setting up of a cerebral lesion model in a non-human primate, the marmoset, where the functional motor recovery can be assessed in order to study thereafter the effect of neuro-implant. Methods: 14 marmosets served to characterize the new lesion model induced by stereotaxic injection of a toxin inhibiting the cellular metabolism. Behavioral tests assessing the neurological score, dexterity and pulling strength of the upper limb, could assess the functional recovery in the acute, sub-acute and chronic phases until 6 months after the lesion. The longitudinal structural and functional follow-up after the lesion and during the recovery was done with MRI (T1, T2, EPI, DTI). The follow-up of the integrity of the CST was studied for the first time in the marmoset with a technic (ME-MRI, manganese-enhanced-MRI) using a contrast agent injected directly in the cortex M1, taken up by neurons and that traced neuronal tracts. A pilot study on 3 marmosets tested the effect of micro-patterned neuro-implants in the cerebral lesion associated with the injection of chondroïtinase ABC (enzyme of extracellular matrix degradation).