The implant itself is a much easier surgery than the one used for deep brain stimulation, with much lower risk of side effects. The device is relatively superficial, placed right under the vertebrae on the surface of the spinal cord. “It’s a very easy, semi-invasive procedure,” Nicolelis says. “In the future, we may be able to do this noninvasively, because there are ways you can actually pass currents through skin and through bone to get these fibers excited.” Nicolelis plans to test the treatment in chimpanzees before initiating human trials. At least one spinal-cord stimulation therapy is already in clinical use to treat chronic pain.
While deep brain stimulation has changed the landscape for late-stage Parkinson’s treatment, it’s still a very complicated, expensive, and deeply invasive procedure, says Patrick Aebischer, president of the Swiss Federal Institute of Technology, in Lausanne. “If you could do this in humans, it would be a fantastic step,” he says, making electrical stimulation available to a much wider group of patients. A noninvasive device would be even more appealing: “If you could do this transcutaneously, you’d change the whole ball game,” Aebischer says. “It opens up a very interesting new possibility for using electrophysiology to treat Parkinson’s disease.”
However, the research is in its early days. “We have to keep in mind that these are experimental data,” says Alim Benabid, a professor emeritus of biophysics at Joseph Fourier University, in Grenoble, France, who created the deep brain stimulation technique in the late 1980s. “It is too early to say whether this could replace levodopa treatment or the current deep brain stimulation.” But Benabid is already looking at adding spinal-cord stimulation in his next set of trials, paired with another kind of deep brain stimulation (that of the subthalamic nucleus) in patients with “frozen gait” disorder, who have trouble walking.
Nicolelis isn’t sure how the therapy works, but he believes that by targeting the spinal column–where huge bundles of fibers are responsible for carrying tactile information from the body to multiple targets in the brain–he and his colleagues are creating electrical current that influences dynamics of the whole neural circuit, rather than just a single spot in the brain. “Parkinson’s is a disease of neuronal timing,” he says. “My gut feeling is that this works because it desynchronizes these neurons in the motor cortex and the basal ganglia and other locations. This desynchronizes them, gets them out of phase–almost like it introduces a little bit of noise in the system.”
In focusing on the spinal cord, Nicolelis says, “we’re looking at a very interesting shift in the way you approach the disease. We’re approaching it from a systemic point of view, looking at a whole circuit and gaining access to the whole circuit.” The scientists are now looking to see whether starting spinal stimulation in combination with L-dopa early on could slow or even prevent the progression of disease.