The hope for paralyzed people with injured spinal cords to walk again has always rested on the potential of finding technology to repair severed nerve fibers. Turns out that a good deal of mobility can be regained without actually reconnecting the brain to paralyzed muscles. UCLA scientists have developed a treatment methodology that combines drugs with electric stimulation of the spinal cord, and a bit of forced exercise on the treadmill, to restore much of the leg movement in paraplegic rats.
"Previous studies have tried to tap into this circuitry to help victims of spinal cord injury," he added. "While other researchers have elicited similar leg movements in people with complete spinal injuries, they have not achieved full weight–bearing and sustained stepping as we have in our study." Edgerton’s team tested rats with complete spinal injuries that left no voluntary movement in their hind legs. After setting the paralyzed rats on a moving treadmill belt, the scientists administered drugs that act on the neurotransmitter serotonin and applied low levels of electrical currents to the spinal cord below the point of injury. The combination of stimulation and sensation derived from the rats’ limbs moving on a treadmill belt triggered the spinal rhythm–generating circuitry and prompted walking motion in the rats’ paralyzed hind legs. Daily treadmill training over several weeks eventually enabled the rats to regain full weight–bearing walking, including backwards, sideways and at running speed. However, the injury still interrupted the brain’s connection to the spinal cord–based rhythmic walking circuitry, leaving the rats unable to walk of their own accord. In humans, however, neuroprosthetic devices may bridge spinal cord injuries to some extent, so activating the spinal cord rhythmic circuitry as the UCLA team did may help in rehabilitation after spinal cord injuries.
Press statement from UCLA: UCLA scientists make paralyzed rats walk again after spinal cord injury…
Abstract in Nature Neuroscience: Transformation of nonfunctional spinal circuits into functional states after the loss of brain input
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