Rob Summers is standing up. Two feet on the ground, legs straight, hips squared. He has done it thousands of times before — out of bed in the morning to practice with his championship-winning collegiate baseball team, or up from the couch to get a snack.
Most memorably, he stood up on a July night in 2006 to walk out the door and over to his parked car on a street in Portland, Ore. Standing next to his Ford Explorer, he saw the lights of another vehicle approaching from behind. It was coming fast — too fast.
Before he could get out of the way, the car threw him to the ground, and the driver fled what was a gruesome scene: Summers lay on the asphalt in a pool of blood, the victim of a hit-and-run that severed the connection between his brain and spinal cord and paralyzed him from the chest down.
Fast-forward three and a half years: A 23-year-old Summers is standing up again. He’s in a lab, hooked up to wires and sensors, and surrounded by doctors and research assistants. He is the first patient in an experiment that has gone fantastically right.
When Summers made it to his feet again, Reggie Edgerton, a neurobiologist at the University of California at Los Angeles, waited calmly nearby. As Edgerton had expected, the array of electrodes that researchers had implanted in Summers’ lower back a few weeks prior was effectively reactivating Summers’ limbs by restoring the natural connection between the muscles and the nervous system, which issues the commands for movement. With just a little electricity flowing into his lower spinal cord, Summers’ leg muscles knew exactly how to get to work — without any input from the brain.
For years, scientists had assumed that the spinal cord was nothing more than a glorified telephone line carrying messages to and from the brain. The generally accepted wisdom was that the brain provided instructions for motion, from the voluntary “pick up the ball” to the involuntary “ouch, step off of that sharp tack.”
Cutting the telephonic spinal cord out of the system by severing it completely, or even partially, meant that messages from the control center couldn’t get down to the rest of the body. Paralysis was the end of that conversation; the puppeteer’s strings had been clipped.
But over the course of four decades, and through dozens of experiments, Edgerton and his colleagues have shown that the spinal cord is smart in much the same way the brain is smart: It can, on its own, detect sensory information and send out signals that control the way we move. As Edgerton watched Summers stand straight, decades of research came into view.
It was 1942 when Reggie Edgerton, age 2, was afflicted with infantile paralysis, a disease better known today as polio. It is a viral infection that takes up residence in the spinal cord and brain and attacks the neurons, or nerve cells, responsible for movement. In 1955, 13 years too late for Edgerton, the United States began the widespread use of a new polio vaccine that would eventually prevent millions of children from contracting polio and suffering its consequences.
Today, Edgerton carries only a small physical trace of this childhood bout, in his slightly underdeveloped left arm. But it is difficult not to see the influence — unconscious, he contends — that the experience had on Edgerton’s longtime effort to help the paralyzed walk.
That work took off in the mid-1970s, when Edgerton, then studying the way exercise impacts muscles, learned that Swedish scientists were tracing walking and standing motions directly to nerve signals from the lower spine. Spearheading the work was University of Gothenburg neuroscientist Sten Grillner, who ran chemical experiments on cats, the standard test animal for studying locomotion.
Grillner had severed the cats’ spines, rendering them paralyzed, and then injected them with an amino acid called L-dopa, routinely used to treat Parkinson’s disease — a neurodegenerative disorder of the central nervous system characterized by motor symptoms.
The exact mechanism behind the L-dopa signal is still not completely understood, but one thing was clear: It was effective at getting the spinal cord to send chemical signals that stimulated the cats’ otherwise immobile legs — and not just in a knee-jerk automatic response, but in more complicated steplike, rhythmic patterns. The motion, Grillner determined, was activated by the firing of interneurons — nerve cells that connect sensory neurons to motor neurons — in the lower spinal cord.
Edgerton took a six-month sabbatical in 1976 to study these interneurons with Grillner. Still working with cats on L-dopa, Grillner and Edgerton probed the animals’ spinal cords with a small glass electrode. It was meticulous work, but measurements of electrical activity eventually allowed the scientists to map the locations of some of the specific interneurons that were telling paralyzed leg muscles to move.
In another set of studies, the Grillner team severed the spinal cords of kittens shortly after birth. Yet with time and training, the kittens were able to walk again on treadmills, without any L-dopa or electrode stimulation at all. Moving the kittens through repeated stepping motions seemed to help them regain movement. “If the injury occurs early after the birth, there’s a much greater chance of recovery,” explains Edgerton. The neonatal nervous system has some unique abilities to repair.”
That made him wonder: Would adults with complete spinal injuries, whose bodies heal less readily, ever be able to recover? Would it still be possible to train their spinal cords to learn how to walk again? “When I came back to UCLA,” Edgerton says, “I wanted to focus on this issue completely.”
In 1978, back in his lab at UCLA, Edgerton began a series of experiments on adult cats whose spinal cords were severed. With their torsos slumped into tiny vests attached to a bar, the paralyzed cats were positioned with their hind paws on a treadmill. With the treadmill turned on, the cats’ hind legs went trotting along. Remarkably, the motor neurons still knew how to send walking orders to the legs. Edgerton concluded that the sensory signal to walk was coming from weight on the paws, instead of from the brain.
Others in the field chalked up these results to reflexes, much like the involuntary motion that occurs when a doctor taps your knee. But by the late 1980s, advanced pharmacology allowed Edgerton to prove them wrong: To do so, he injected paralyzed cats with strychnine, a toxin commonly used in rat poison.
Strychnine blocks glycine, an amino acid that inhibits nerve function in the brain stem and the spinal cord. With the glycine shield gone, neural activity went up. Within half an hour, cats that had been paralyzed for three months began walking as if their spinal cords were intact — this was hardly a reflex effect.
“We showed that a spinal cord could learn if you expose it to a training paradigm,” says Edgerton. “The training provides stimulus. If you stop training it, it forgets how to step.”
By the early 1990s, Edgerton and his team decided to see if they could teach the human spinal cord some lessons as well. Their subjects were patients with partial and complete spinal cord injuries. Only those with partial injuries showed improvement with physical therapy, including regular assisted walking and guided leg exercises on the treadmill.
Many ultimately regained voluntary control of their leg muscles, standing up and even walking on their own. The exercise, researchers presumed, rebuilt the connection between the brain and the spinal cord, awakening, or even regrowing, the locomotive neural circuits the injured patient had lost.