Restoring voluntary control of locomotion after paralyzing spinal cord injury

Science. 2012 Jun 1;336(6085):1182-5. doi: 10.1126/science.1217416.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / physiology
  • Brain Stem / physiology
  • Dopamine Agonists / administration & dosage
  • Electric Stimulation
  • Female
  • Gait
  • Hindlimb / physiology*
  • Locomotion*
  • Motor Cortex / physiology*
  • Nerve Fibers / physiology
  • Neuronal Plasticity
  • Neurons / physiology
  • Paralysis / physiopathology
  • Paralysis / rehabilitation*
  • Pyramidal Tracts / cytology
  • Pyramidal Tracts / physiology*
  • Rats
  • Rats, Inbred Lew
  • Recovery of Function
  • Robotics*
  • Serotonin Receptor Agonists / administration & dosage
  • Spinal Cord / cytology
  • Spinal Cord / physiology
  • Spinal Cord Injuries / physiopathology
  • Spinal Cord Injuries / rehabilitation*

Substances

  • Dopamine Agonists
  • Serotonin Receptor Agonists