When Garrett came to visit his mother in the hospital the day her gallbladder was removed, he probably never imagined he would end up staying. He was a robust college wrestler, and aside from a little headache and cough, he didn’t feel very sick. But his feet had been falling asleep, and he had a tingly feeling in his hands. He’d been dragging all month, and he felt so weak that he actually fell as he was leaving the hospital.
So the doctors admitted Garrett for observation. They found he couldn’t push or pull his arms with as much strength as a normal 18-year-old, and he could barely lift his legs. When they asked him to touch his nose, his fingers trembled, and when they tapped his tendons with a reflex hammer, his muscles barely responded.
After five days, Garrett hardly had enough strength to breathe. Doctors put a tube down his throat into his airway and connected him to a ventilator. Two days later, they transferred him from the community hospital to the pediatric intensive care unit at our advanced tertiary care hospital.
To solve the mystery of Garrett’s condition, doctors gave him special tests that stimulated his nerves with tiny electric jolts to see whether the nerves’ “messages” would be conveyed with normal speed and amplitude to his muscles. They weren’t. Garrett’s arm and leg weakness and the abnormal nerve studies pointed to Guillain-Barré syndrome.
The disorder affects about one or two in every 100,000 people worldwide each year, and except for head injuries and stroke, it is the chief cause of sudden paralysis in all age groups since the advent of polio vaccine. A half century ago, poliomyelitis affected 25 in every 100,000 people in the United States and left 21,000 patients a year paralyzed. What differentiates polio from Guillain-Barré syndrome is that polio patients, mostly children, tend to develop an asymmetrical paralysis with no sensory loss. In patients with Guillain-Barré syndrome, both paralysis and sensory changes appear, ascend symmetrically from the tips of the toes and fingers to the body’s core, and then largely disappear several weeks later. Another major difference was discovered by physicians Georges Guillain, Jean-Alexandre Barré, and Andre Strohl during World War I while treating two French soldiers. They found that the fluid cushioning the patients’ spinal cord showed an abnormal increase in protein—just as with polio—but no increase in infection-fighting white blood cells. And while researchers showed that a virus causes polio, they could not find an infectious cause for Guillain-Barré syndrome.
It took another 40 years to discover what does underlie the disorder. The answer came when experimenters succeeded in creating a model for the disease in rodents by inducing an allergy to nerve tissue. Further research confirmed that in Guillain-Barré syndrome the body mistakenly attacks some aspect of the nervous system—in essence, the body develops an allergy to a part of itself.
The most common target seems to be a protein called myelin. Myelin insulates the long projections of nerve cells. It multiplies the speed with which electrical signals travel up and down the long nerve-cell axons, instantly converting a thought into a movement and a pinprick into a sensation. When the immune system attacks and destroys myelin, the impulses that control movement and sensation slow down and sometimes stop. The longer the nerve-cell axons extend, such as to reach the feet or hands, the earlier and more severely the syndrome affects them.
