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A paper was published this week from the Gregoire Courtine lab in Switzerland. Courtine, who we have discussed here in recent months, studies activity and its role in recovery. Much of Courtine’s science was shaped by his years as a graduate student under Reggie Edgerton at UCLA. Edgerton’s lab is one of seven in the Reeve International Research Consortium for Spinal Cord Injury; Courtine was an Associate in the Consortium.

This paper is titled “Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury.”

The gist of it this: spinal cord injury causes progressive damage in the chronic phase, which Courtine and his group observe during assisted locomotion (using a harness suspended over a treadmill). From the abstract:

Severe spinal cord injury in humans leads to a progressive neuronal dysfunction in the chronic stage of the injury. This dysfunction is characterized by premature exhaustion of muscle activity during assisted locomotion, which is associated with the emergence of abnormal reflex responses.

Why does this happen?

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