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? Courtine postulates that the spinal cord is plastic, that is, it continues to adapt and modify its structure to compensate for loss of neurons. This plasticity, however, is undirected and thus forms “aberrant” connections that make the wrong kinds of connections. From the abstract:
We evaluated alterations in functional, electrophysiological and neuromorphological properties of lumbosacral circuitries in adult rats with a staggered thoracic hemisection injury. In the chronic stage of the injury, rats exhibited significant neuronal dysfunction, which was characterized by co-activation of antagonistic muscles, exhaustion of locomotor muscle activity, and deterioration of electrochemically-enabled gait patterns. As observed in humans, neuronal dysfunction was associated with the emergence of abnormal, long-latency reflex responses in leg muscles.
After analyzing the circuitry below the spinal cord injury, Courtine et al, report that the remodeled networks revealed
“... significant correlations between the development of neuronal dysfunction, emergence of abnormal reflexes, and anatomical remodeling of lumbosacral circuitries. Together, these results suggest that spinal neurons deprived of supraspinal input [from the brain] strive to re-establish their synaptic environment. However, this undirected compensatory plasticity forms aberrant neuronal circuits, which may engage inappropriate combinations of sensorimotor networks during gait execution.
What does this mean? Optimal gait retraining will have to deal with networks that may be getting rewired in counterproductive ways. The question that remains, then: Might this plasticity be better managed?