Restoring Voluntary Control of Locomotion after Paralyzing Spinal Cord Injury
Restoring Voluntary Control of Locomotion after Paralyzing Spinal Cord Injury
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DOI：
10.1126/science.1217416
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发表时间：
2012-06-01
期刊：
影响因子：
56.9
通讯作者：
Courtine, Gregoire
中科院分区：
文献类型：
--
作者：
van den Brand, Rubia;Heutschi, Janine;Courtine, Gregoire
一半的人类脊髓损伤会导致慢性瘫痪。在这里，我们介绍了一种电化学神经假体和机器人姿势接口，旨在鼓励脊髓上介导的运动与瘫痪病变的大鼠。尽管直接的脊髓上通路被中断，皮质仍恢复了将上下文信息转化为特定任务命令以执行精细运动的能力。这种恢复依赖于皮质投射的广泛重塑，包括脑干和椎管内中继的形成，这些中继恢复了对电化学激活的腰骶部电路的定性控制。自动化的限制性训练，不涉及皮层神经元，未能促进translesional可塑性和恢复。通过鼓励在功能状态下的积极参与，我们的训练模式引发了一种依赖于皮层的恢复，这种恢复可能会改善人类在类似损伤后的功能。
Half of human spinal cord injuries lead to chronic paralysis. Here, we introduce an electrochemical neuroprosthesis and a robotic postural interface designed to encourage supraspinally mediated movements in rats with paralyzing lesions. Despite the interruption of direct supraspinal pathways, the cortex regained the capacity to transform contextual information into task-specific commands to execute refined locomotion. This recovery relied on the extensive remodeling of cortical projections, including the formation of brainstem and intraspinal relays that restored qualitative control over electrochemically enabled lumbosacral circuitries. Automated treadmill-restricted training, which did not engage cortical neurons, failed to promote translesional plasticity and recovery. By encouraging active participation under functional states, our training paradigm triggered a cortex-dependent recovery that may improve function after similar injuries in humans.