Multiple sclerosis, MS, is a disease that has been hard for us to understand because we just haven’t had enough basic knowledge, basic knowledge of biological processes like genetics and immunology, but we’re coming.

MS is the most common disease of the nervous system young adults can get. We know people aren’t born with it but it does run in families. Relatives of patients with MS are eight times more apt to get it than others. We know it is five times more common in the temperate zones of Europe and America than in the tropics, yet there is something odd about this figure. The relative risk of getting MS seems to depend on what the climate was in whatever place you spent the first 15 years of your life. If you lived in the tropics until age 15, then moved to Maine, your risk is as low as it would be if you had stayed in the tropics. On the other hand, if you were brought up in Maine, then moved to tropical Brazil in your teens, your risk stays as high as it would be if you had never left.

That’s hard to explain. Scientists usually speculate that MS victims are born with something wrong with their immune systems, something that never shows up unless the immune system is triggered by a virus infection contracted during the first 15 years of life. Perhaps the virus is one of the “slow” viruses and one that is rare in the tropics. There is very little proof to support that theory, but scientists haven’t had enough knowledge to offer a better one.

Whatever the cause, the disease attacks a specific part of nerve fibers, the myelin sheath. Nerve cells carry messages for long distances just as telephone cables do. Like the copper wires in telephone cables, nerve fibers have to be separated by insulation to prevent the messages from interfering with each other. Myelin is the material the body makes to insulate nerve fibers. In MS the body starts destroying this myelin insulating sheath, and the myelin gets replaced by scar-like (sclerotic) tissue. This scarring, or sclerosis, can occur anywhere there is myelin, and it usually occurs in more places than one. That’s how it came to be called multiple sclerosis.

That also explains why the symptoms can be so different from one patient to the next. One patient might have a scarring of the nerve leading to one of the muscles that moves the eyeball so the muscle becomes weakened or even paralyzed. If the eyeballs can’t move together the result is double vision. Another patient might have loss of the nerve supply to some of the muscles of the legs and have to spend the rest of his or her life in a wheelchair. One woman I know had just a patch of numbness at the base of her thumb for years. Damage to myelin in the brain can cause fatigue, true vertigo with a spinning sensation, muscle incoordination and clumsiness, speech that is slurred as if the patient were drunk, and even unexplained mood changes. The first patient with MS I ever saw, way back in medical school, was the happiest person in the hospital despite being bedridden and near death from her disease.

Another strange thing about MS is how differently it progresses in different people. About a third of its victims show no visible evidence of disease and go about their business without even their neighbors knowing they are sick. They may live out their normal life span and die of something unrelated to MS. About one in 20 has a rapidly progressive downhill course, becoming bedridden by paralysis within a year and dying within five years. The rest of the patients fall between these extremes. Typically the patient, more often a woman than a man, is in her thirties when the first attack occurs. Whatever the symptoms, whether double vision, or numbness, or paralysis, or what have you, things get better with time. The next attack may come weeks or months or years later and may affect an entirely different part of the body.

A couple of years ago researchers at the Albert Einstein College of Medicine in New York City produced an MS-like illness in guinea pigs by injecting them with a myelin-containing extract from the spinal cords of other animals. The immune systems of guinea pigs reacted to this foreign protein just the way they would react to an invasion of germs: They developed antibodies to it. These antibodies took care of the foreign protein just the way they are supposed to, but then they began attacking the guinea pigs’ own myelin. They had become immune to their own tissue and their antibodies attacked their myelin just as if it had been germs. This is approximately what we think happens in human MS, and it produced a very similar disease in the guinea pigs. Dr. Cedric Raines and his colleagues at Einstein have been able to reverse the disease process by injecting these guinea pigs with the building blocks of myelin. Whether this can ever be developed into a treatment for human MS will require undetermined years of further study.

Using a different approach, Drs. Vanda Lennon and Moses Rodriguez of the Mayo Clinic infected mice with a virus called Theiler’s murine encephalomyelitis virus. This results in destruction of myelin and an MS-like disease in the mice. Earlier, the Mayo group had been able to isolate an antibody from healthy mice injected with spinal cord tissue just the way the Einstein group had done with their guinea pigs. They injected this antibody into their afflicted mice, expecting this would hurry the disease process along. Instead, the mice started getting better. When they examined spinal cord tissue from these recovering mice under the microscope, they found new myelin forming around the damaged nerve cells.

That little surprise is going to require us to rethink our whole concept of MS. Is this evidence of a battle going on in MS between good antibodies and bad antibodies? If so, what can we do to help the good guys? Again, it will be several years before the answers to these questions can lead to effective treatments for MS, but after years of hearing nothing, it’s nice to know they’re making progress.

Robert A. Graves, M.D. is a retired physician who lives in Orono. His column appears biweekly.