During the seventies and eighties, he remained “hunched over a sort of periscope, peering down a little green tube,” as he wrote in an unpublished memoir, trying to answer his own question: How does a neuron’s axon find its way to its appropriate target? Neurons are only a portion of what is cumulatively called a “nerve bundle”; they carry the electric impulses that govern muscle contraction or register sensation. But neurons are surrounded by various kinds of ancillary cell, grouped under the name of glia (modern Latin for “glue”). Glial cells vastly outnumber nerve cells. When Raisman began investigating paralysis, no one knew what the glial cells did, though there were hints that their role was significant. “Einstein’s brain had an unusually high proportion of glial cells,” he points out. “Could it be a coincidence? We’d have to kill a lot of geniuses to find out.”
At the time, glial cells were considered the brain’s equivalent of junk DNA, and most neuroanatomists were not interested in them. They seemed to hold little promise in spinal-cord repair; in fact, they appeared to play a contrary role. After an injury, a chain of responses takes place in the spine: broken blood vessels swell, killing off neurons that end up squeezed within the cage of the vertebrae. Other neurons, sensing that the central nervous system has been breached, commit suicide; still others sprout new axons that struggle to reëstablish severed connections. Glial cells appear to hinder this regeneration process: they rush to create a physical barrier, sealing the spinal cord with scar tissue that neurons cannot penetrate. According to many researchers, the glial cells that form the scar are toxic to growing nerves.
But Raisman realized that there is one part of the central nervous system where glial cells encourage regeneration: in the nerves that connect the nose to the brain. The nerves of the nasal cavity regrow when they are damaged or cut, and this healing is directed by special glial cells, which usher neurons along the path from the nose membrane to the brain. When nerves in the nose die, after three months or so, new ones spring forth, allowing people to maintain the ability to smell. In the nineteen-nineties, Raisman damaged the spines of rats with a tiny needle heated at the tip, and then inserted the special glial cells—olfactory ensheathing cells—at the site of the wound, to see what would happen.
As I sat in his corridor, he showed me a short movie that he had made some years ago. It features footage of an unnamed white rat crosscut with video of his granddaughter Amy when she was about a year old. (He noted that his daughter, Ruth, wasn’t thrilled about the juxtaposition.) “Off you go, Amy,” Raisman said to the screen, clicking the play button with excitement. In the video, the toddler crawls up the stairs of her house. But it is not Amy whose crawling you are meant to be excited about; it is the rat that is climbing in subsequent images. Raisman had severed the nerve in its spine that controlled its front left paw, then introduced olfactory ensheathing cells to heal the wound. The movie shows the rat before and after the procedure. In the first shot, the rat, favoring its left paw, is unable to grasp the bars of its cage as it tries to climb out. In the second shot, the rat scampers up the side of the cage “with aplomb,” as Raisman put it to me. He then recalled the story of the day he had noticed the animal’s striking recovery. One evening at midnight, he had gone to visit the lab’s rat enclosure—“Rats are more active in the night,” he explained—and held out a bit of crushed Chinese egg noodles. “It put its paw right out and took the food, and realized it could do it, and I realized we had done it,” he says. “To the best of my knowledge, it was the first evidence ever that you could get spinal reconnection.” The pleasure of that moment hadn’t dimmed in almost twenty years. “That rat convinced me,” he says. “That was the eureka moment, I would say, of my existence.”
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In April, 2012, Tabakow, with his medical team, opened up Fidyka’s skull and removed part of his olfactory bulb. The human sense of smell is not very acute, so the olfactory bulb is relatively small—about the size of a sunflower seed. (A goat’s is larger.) Tabakow and his associates next sliced the extracted tissue into two-millimetre sections, isolated the olfactory ensheathing cells, and then gave them almost two weeks to subdivide, in order to have enough cells—half a million—for the operation. Then he opened Fidyka’s spine around the T9 vertebra and made almost a hundred microinjections to situate the cells above and below the wound. He placed more of the cells onto a strip of nerve tissue that he’d extracted from Fidyka’s lower leg and inserted in his spine, in order to help span the gap in his cord. Tabakow closed the incision, and within a few weeks his patient was beginning his real rehabilitation.
- A paraplegic undergoes pioneering surgery
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