Both Cause and Cure of Multiple Sclerosis Still Elude Scientists
During the last 50 years, gold, snake venom and oil of evening primrose have all been touted as cures for multiple sclerosis. So have yeast, sunflower seeds and surgical implants of pig brains.
All the remedies have one thing in common. None works.
In recent years, scientists have looked at radiation, pressurized oxygen and transplant drugs in search of something that will stop the often inexorable destruction caused by this disease. But the answer, sadly, is much the same.
Nothing has been shown to cure multiple sclerosis or even convincingly slow it down. Perhaps even worse, no one knows what causes it.
250,000 American Cases
About 250,000 Americans have multiple sclerosis. The disease destroys the insulation, a substance called myelin, that surrounds nerve fibers. As a result, nerve messages get distorted or fail to go through. Victims have trouble controlling their movements. Often they can not walk. Symptoms can include tremors, blurred vision, weakness and slurred speech.
“The treatment in this disease hasn’t changed dramatically in the last 25 or 30 years,” said Dr. Floyd Davis of Rush Medical College in Chicago. “We’ve all seen new approaches, and a lot of promising things have happened. But nothing has really changed the conventional way in which we deal with patients.”
This does not mean the odds of conquering multiple sclerosis are entirely hopeless. Plenty of scientific research is going on. There are hints, still far from proven, that it may yet be possible to stop the destruction by tinkering with the bodily parts that have run awry.
In fact, a cancer drug called cyclophosphamide clearly helps, even though its benefits are temporary and it is too toxic for many patients to consider using. Yet it has provided the first evidence that it is even possible to interrupt the disease.
Other new studies suggest that a natural hormone called beta interferon might do some good. The most widely publicized approach of recent months is a synthetic protein called Cop 1. In preliminary studies, it seems to halt and even reverse the mild early stages of multiple sclerosis.
Cop 1 is especially interesting because it does not cause bad side effects. But experts generally are reluctant to get excited about this drug until several large, carefully controlled studies show that it works.
Reason to Be Skeptical
They have good reason to be skeptical. Time after time, therapies described glowingly in early reports have turned out, years later, to be worthless.
One recent example is hyperbaric oxygen. A report four years ago in the New England Journal of Medicine said breathing pure oxygen in a pressurized chamber seemed to relieve the disease. Storefront oxygen clinics opened up around the country. Demand, at least for a while, was brisk. However, several new follow-up studies have found no value in this treatment.
Hopes raised and smashed are a way of life for people with multiple sclerosis.
“They are motivated by hope, but they have become a great deal more skeptical, and justifiably, because they have been disappointed any number of times,” said Dr. Byran H. Waksman of the National Multiple Sclerosis Society. “At the same time, I think they ought to be optimistic.”
Sometimes the disease grows steadily worse from the start. More often, though, victims suffer erratic spurts when new symptoms suddenly flair up and then recede.
One major research goal is to figure out what causes multiple sclerosis, a crucial step for finding strategies to cure it. Evidence is growing that people may inherit a genetic susceptibility to the disease. Studies have shown that identical twins are far more likely than fraternal twins to share the disease.
Recently, Dr. Dessa Sadovnick of the University of British Columbia found that children of people with multiple sclerosis have about a 5% chance of getting it themselves. This is 50 times higher than the risk for the general population.
Just what triggers the disease is still unclear, although many experts subscribe to one of several viral theories. Probably the leading one is the idea that some tiny portion of myelin is identical to a virus. The body mounts a routine immune defense to fight off the germ, perhaps the measles or flu virus. But in a disastrous case of mistaken identity, it attacks the look-alike myelin as well.
Immunity Suppressed
Since the body’s own immune weapons seem to be involved in destroying myelin, some experts have tried out a variety of drugs that suppress immunity. This apparently is how cyclophosphamide works. However, many view this kind of tactic as unacceptably crude.
“That, philosophically, is an unsatisfactory approach,” Waksman said. “You are taking away a system that the body needs in order to get rid of one of its unhappy byproducts.”
Some instead are tinkering with more precise assaults on the immune system, trying to disarm the specific cells that do the damage. One approach is to craft antibodies that zero in on the suspected culprits. Another is to remove a victim’s immune cells, inactivate them, and then inject them back into the patient, where, if all goes well, they might serve as a vaccine against multiple sclerosis.
While beta interferon seems to interrupt the disease, experts are also intrigued by another form of the substance, called gamma interferon, that appears to make multiple sclerosis worse, not better. This may provide an important clue about the underlying defect in multiple sclerosis.
Since there is no cure, the goal of doctors treating multiple sclerosis patients is to ease their symptoms. A hormone called ACTH is widely used to shorten attacks. Other drugs help control seizures, bladder problems, depression, spasticity and other common signs of the disease. Researchers are also working on medicines that seem to boost nerve signals, so multiple sclerosis victims can do more with what they have left.
But the central goal of multiple sclerosis research is to stop the disease and cure it. Despite the legacy of failure, many researchers are convinced that they will eventually do this.
“We are learning more each year,” Davis said. “There is no question this disease will be cracked someday. It will probably happen very quickly. We’ll all look back on it and say, ‘Wow! Why didn’t I think of that?’ ”
