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Restoring voluntary control of locomotion after paralyzing spinal cord injury


van den Brand, R; Heutschi, J; Barraud, Q; DiGiovanna, J; Bartholdi, K; Huerlimann, M; Friedli, L; Vollenweider, I; Moraud, E M; Duis, S; Dominici, N; Micera, S; Musienko, P; Courtine, G (2012). Restoring voluntary control of locomotion after paralyzing spinal cord injury. Science, 336(6085):1182-1185.

Abstract

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.

Abstract

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.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2012
Deposited On:29 Nov 2012 10:20
Last Modified:05 Apr 2016 16:07
Publisher:American Association for the Advancement of Science
Series Name:Science
ISSN:0036-8075
Publisher DOI:https://doi.org/10.1126/science.1217416
PubMed ID:22654062

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